Total dietary regulation in the treatment of diabetes

MONOGRAPHS OF

THE ROCKEFELLER INSTITUTE

FOR MEDICAL RESEARCH

No. 11 October 15, 1919

TOTAL DIETARY REGULATION IN THE TREATMENT
OF DIABETES

By

FREDERICK M. ALLEN, M.D., EDGAR STILLMAN, M.D., and
REGINALD FITZ, M.D.

NEW YORK

The Rockefeller Institute for Medical Research

1919

LIBRARY

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ITHACA, N. Y.

3 1924 104 225 283

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Library

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http://www.archive.org/details/cu31924104225283

MONOGRAPH No. 11

TOTAL DIETARY REGULA'
TION IN THE TREATMENT
OF DIABETES.

BY

FREDERICK M. ALLEN, M.D., EDGAR STILLMAN, M.D., AND
REGINALD FITZ, M.D.

NEW YORK
The rockefeller institute for medical research

igi9

|<H^ '■4-4-L

PREFACE.

This monograph comprises the records of seventy-six out of one
hundred diabetic patients treated in the Hospital of The Rockefeller
Institute, and chapters on certain aspects of the clinical research.
The opening chapter was written as an introduction to the publication
as originally planned, and was to have been followed by chapters deal-
ing respectively with carbohydrate, protein, fat, total metabolism,
acidosis, pathology, etc., with combined animal and clinical experi-
ments, and a fairly complete survey of the hterature. Certain events,
however, have interfered with this program and publication is proceed-
ing in reverse order, the clinical part now appearing in advance of the
reports of the animal experiments. The latter will shortly appear in
a series of journal articles. Most of the collected bibliography, except
that pertaining to the history of the subject (Introduction) , has like-
wise been omitted from the present monograph. Reports by members
of the staff of this hospital, concerning chemical aspects of the dia-
betic problem or methods employed, are included in the bibUography
of Chapter I under the names of CuUen, Fitz, Pahner, Stilhnan, and
Van Slyke. The cooperation and courtesy received so liberally from
outside the Institute are acknowledged in the text as far as possible.

When publication is complete, it will be seen that the conclusions
rest upon a unified research composed of three principal interde-
pendent parts. One of these has compared clinical diabetes in its
principal characteristics with that produced experimentally in various
species of animals, and has shown that the latter, in the absence of
spontaneous tendencies, is influenced by changes in the total metab-
olism and body weight, and not by carbohydrate ingestion alone.
The second is the present chnical investigation, in which this principle
has been applied to patients. The third is a pathological study, not
yet finished, but included here in the form of a preliminary outline
because of its' important relation to the problems of treatment.

IV PREFACE

A therapeutic advance should mean a raising of the general level of
chnical results, in the sense of saving hfe in some proportion of cases
formerly fatal, and prolonging it to greater or less extent in the more
hopeless cases. Expectations of an actual cure, in the sense of a
restoration of the normal power of food assimilation, will necessarily
be disappointed in most cases under any dietetic treatment, and the
need of some more potent therapy than diet is a keen stimulus to
research. The method of treatment here presented has never been
proposed as such a cure, and ameHoration of the existing condition
and preservation of hfe and usefulness at the price of continued pre-
cautions have been recognized as the limit of present attainment in
diabetes. As set forth in the text, the mistakes incident to the
development of a new method have reduced the general results below
the theoretical ideal. The severity of the test is evident, however,
from the grave character of the cases chosen and their known fate
under former practice. The experience as a whole is believed to sus-
tain both the theoretical principle and its practical value for the
dietetic treatment of diabetes.

MONOGRAPH OP THE ROCKEFELLER INSTITUTE FOR MEDICAL RESEARCH,

NO. 11, October 15, 1919.

TOTAL DIETARY REGULATION IN THE TREATMENT OF

DIABETES.

By FREDERICK M. ALLEN, M.D., EDGAR STILLMAN, M.D., and REGINALD

FITZ, M.D.

{From the Hospital of The Rockefeller Institute for Medical Research.)
(Received for publication, April 29, 1918.)

CONTENTS.

Chapter I. Introduction. History 1

The Ancient Period (to 1675 A. D.) 2

The Second or Diagnostic Period (1675-1796) 8

The Period of Empiric Treatment (1796-1840-50) 14

The Modern or Experimental Period 21

Bibliography 65

Chapter II. General Plan of Treatment 79

General Measures 80

Routine Care of Patients 80

Ward Regulations and Clinical Remarks 82

Treatment up to Cessation of Glycosuria in Simple Cases 90

Emergencies and Complications 98

Acidosis 98

Infectious and Surgical Complications 115

Treatment following Cessation of Glycosuria 125

Ideals of Diet and Laboratory Control 137

Practical Management of Diets 148

Organization 148

Equipment 149

Special Features of Maintenance Diet 151

General Scheme and Specimen Diets 161

Food Tables 173

Chapter III. Case Records and Charts 177

Chapter IV. Pancreas Feeding 461

Chapter V. Exercise 468

Immediate Effect of Exercise on Blood Sugar 468

The Effect on Carbohydrate Tolerance and Glycosuria 488

The Use of Exercise in Various Classes of Patients 491

The More Permanent Effects of Exercise upon Assimilation and the
Diabetic Condition 495

V

VI CONTENTS

Chapter VI. The Influence of Fat in the Diet 500

Influence of Body Weight 501

Influence of Total Diet 502

Chapter VII. Results — Prognosis 532

Severity of Cases 532

Cases and Results by Decades 536

Causes of Death 557

Treatment of Coma 558

Infections 562

Reasons for Failure in Treatment 567

Severity of the Treatment 575

Prognosis 577

" Spontaneous Downward Progress" 581

General Summary 594

Chapter VIII. Etiology and Pathology 596

Etiology 596

Carbohydrate or Dietary Excess 596

Obesity 598

Pluriglandular Disorders 599

Constitutional Defects 600

Heredity. . . . : 600

Nervous Causes 605

Trauma 607

Infection and Inflammation 608

Pathology 615

Changes Causing Diabetes 615

Changes Due to Diabetes 620

Clinical Application 631

Chnical Etiology 631

Anatomic Diagnosis 636

Relation to Treatment 642

Conclusions 646

CHAPTER I.

INTRODUCTION.

History.

Understanding of the existing state of a subject is generally aided
by knowledge of its history. Aside from what is given in text-books,
notably those of Cantani and Lepine, the early history of diabetes has
been written briefly by Hirsch, but most exhaustively by Salomon, to
whom reference may be made for exact citations of most of the ancient
and medieval works here quoted. A previous publication^ has re-
viewed some of the theoretical and experimental features of the sub-
ject. The following account aims to trace the development of clinical
knowledge and treatment of diabetes, taking note of theories and ex-
periments only as they have influenced practice. The attempt has
been made to present the true and significant, assigning credit to the
successive workers as accurately as the recorded evidence permits.

It is convenient, following approximately Cantani, to divide the
history of diabetes into four periods. The first extends from the most
ancient times to the discovery of the sweetness of the urine by Willis
in 1675, which ushered in the second or diagnostic period. The third
period, that of empiric treatment, began with Rollo in 1796. The
fourth, or modern period, was inaugurated in the decade 1840 to 1850,
the most prominent founders being Bernard and Bouchardat. With
all its imperfections, this yet merits the name of the experimental
and scientific period.

»Men(l).

I. The Ancient Period (to 1675 A. D.).

"In the papyrus Ebers, which is a copy of an Egyptian medical
compilation already old in the time of Moses, there is mention of
polyuria, and it is hard to conceive that such a marked departure from
health could at any time have escaped observation" (Saundby). For
explanation of the relatively late period of human history at which
diabetes was first clearly recognized and described, we need not as-
sume the absence or rarity of the disease among the ancients, but must
rather consider the impossibility of their diagnosing mild cases, the
natural confusion of severe cases with chronic nephritis and various
forms of pol3mria and with tuberculosis and other wasting conditions,
and the further difl&culties presented by the various complications.
The differences between cases have puzzled even modern physicians
to such an extent that the existence of diabetes as a unified entity
rather than a disjointed symptom-complex has been disputed up to
very recent years.

Hippocrates (460-377 B.C.) made no mention of any condition
clearly recognizable as diabetes. A notion concerning the quantity of
urine, in a passage translated by Richardson from the third book of
the Epidemics,^ is like that of Celsus, but the first known recognition
of diabetes occurred at about the height of the Roman power.

Aulus Cornelius Celsus (30 B.C.-SO A.D.) wrote as follows:'
''When urine, even in excess of the drink, and flowing forth without

^ "In some cases the urine was not in proportion to the drink administered, but
greatly in excess ; and the badness of the urine was great, for it had not the proper
thickness nor concoction nor purged properly; for in many cases purgings by the
bladder indicated favorably, but in the greatest number they indicated a melting
of the body, disorder of the bowels, pain and a want of crisis."

'Lib. iv, cap. xx, 2; ref. by Salomon: "At cum urina super potionum modum
etiam sine dolore profluens maciem at periculum facit, si tenuis est, opus est
exercitatione et frictione, maximeque in sole, vel ad ignem; balneum rarum esse
debet, nequelonga in eo mora; cibus comprimens; vinum austerum meracvun, per
aestatem frigidum, per hiemem egelidum; sed tantum, quantum minimum sit.
Infima alvus quoque vel ducenda, vel lacte purgenda est. Si crassa urina est

2

HISTORY 3

pain, causes emaciation and danger, if it is thin, exercise and massage
are indicated, especially in the sun or before a fire; the bath should be
infrequent, nor should one linger long in it; the food should be con-
stipating, the wine sour and unmixed, in summer cold, in winter luke-
warm; but everything in smallest possible quantity. The bowels also
should be moved by enema, or purged with milk. If the urine is
thick, both exercise and massage should be more vigorous; one should
stay longer in the bath; the food should be light, the wine likewise.
In each disease, all things should be avoided that are accustomed to
increase urine."

In this compressed passage, Celsus gives the first description of
diabetes, introduces an error (fluid output greater than intake)
destined to endure eighteen centuries, and touches some modern treat-
ment. It is not known to what extent this knowledge was original
with Celsus or handed down by predecessors. At any rate, the recog-
nition of the disease was so new that it had not yet received a name.

Aretaeus of Cappadocia (30-90 A.D.), living under the emperor
Nero, and writing in Ionian Greek, was the second to describe dia-
betes, and the first known to have called it by the name {ha^alvav, to
run through; Sta/S^rijs, a siphon). In a passage translated by Schn6e*,

vehementior esse debet et exercitatio et frictio; longior in balneo mora; cibisopus
est tenuis; vinum idem. In utroque morbo vitanda omnia sunt, quae urinam
movere consuerunt."

^ "Diabetes is a strange disease, which fortunately is not very frequent. It con-
sists in the flesh and bones running together into urine. It is like dropsy in that
the cause of both is moisture and coldness, but in diabetes the moisture escapes
through the kidneys and bladder. The patients urinate unceasingly; the urine
keeps running like a rivulet. The Ulness develops very slowly. Its final outcome
is death. The emaciation increases very rapidly, so that the existence of the
patients is a sad and painful one. The patients are tortured by an unquenchable
thirst; they never cease drinking and urinating, and the quantity of the urine ex-
ceeds that of the liquid imbibed. Neither is there any use in trying to prevent the
patient froni urinating and from drinking; for if he abstains only a short time from
drinking his mouth becomes parched, and he feels as if a consximing fire were raging
in his bowels. The patient is tortured in a terrible manner by thirst. If he re-
tains the urine, the hips, loins, and testicles begin to swell; the swelling subsides as
soon as he passes the urine. When the illness begins, the mouth begins to be
parched, and the saliva is white and frothy. A sensation of heat and cold extends
down into the bladder as the illness progresses; and as it progresses still more there

4 CHAPTER I

Aretaeus outlines some of the principal symptoms, the progressive
course, and the fatal prognosis. He anticipates modem conceptions
of a failure of assimilation, conversion of tissue into urinary products,
and possible origin of some cases in acute infections. He was retro-
grade in treatment, for he advised a non-irritating diet of milk and
carbohydrates, andhiera, nardum, mastix, and theriak (opium? sugar?)
as drugs. He is commonly credited with being the first to regard
diabetes as a disease of the stomach; but his vague notion of a dis-
order akin to ascites hardly entitles him to a claim upon this false idea
which was productive of so much truth in the period from Rollo to
Cantani.

Claudius Galenus (born 131 A.D.) saw two patients and introduced
two ideas: first, that diabetes is a weakness of the kidneys, which can-
not hold back water and also are thirsty for fluid ; second, that the urine
consists of the unchanged drink. Galen's great authority maintained
these errors for about 1500 years, and retarded progress in the knowl-
edge of diabetes.

Chronological order here shifts the narrative to the Far East.
According to Iwai, the first oriental description of diabetes was given
in the year 200 by Tchang Tchong-king, perhaps the greatest of
Chinese physicians. "There is a disease called 'the disease of thirst,'
in which poljoiria is the characteristic symptom. One may drink as
much as ten Hters per day, which is recovered in the urine." A
Chinese medical work of about the year 600 classifies four supposed
groups of cases, and notes the s}Tnptoms of polyphagia, polydipsia,
and pol5Tiria. Still a later work mentions furunculosis. About the
fifteenth century, diabetes was attributed to wine and high living.

is a consuming heat in the bowels. The integuments of the abdomen become
wrinkled, and the whole body wastes away. The secretion of the urine becomes
more copious, and the thirst increases more and more. The disease was called
diabetes, as though it were a siphon, because it converts the human body into a
pipe for the transflux of liquid humors. Now, since the patient goes on drinking
and urinating, while only the smallest portion of what he drinks is assimilated by
the body, life naturally cannot be preserved very long, for a portion of the flesh
also is excreted through the urine. The cause of the disease may be that some
malignity has been left in the system by some acute malady, which afterward is
developed into this disease. It is possible also that it is caused by a poison con-
tained in the kidneys or bladder, or by the bite of the thirst-adder or dipsas."

HISTORY 5

Among the Japanese, Kagawa Shu-An described the s)m!iptoms of
diabetes as frequency of urination, with urine exceeding the drink in
quantity, pale color and sugar taste of the urine^ and insatiable hunger
and thirst. Homma Gencho in 1864 noted the typical symptoms, the
death from emaciation, and the urine so sweet as to attract dogs.
These accounts show obvious European influence, and the Japanese
seem to have made no original contributions. According to Iwai, this
may be explained by the rarity and mildness of diabetes among them.

In Europe, iEtius of Amida (550 A.D.) accepted the Galenic doc-
trines, but introduced into therapy three measures long used there-
after; viz., bleeding, emetics, and narcotics. According to a passage
quoted from ^tius by Donkin ( (1), p. 128), Archigenes in the second
century was the first to use opium for diabetes.

The earliest mention of the sweetness of diabetic urine is contained
in the Ayur Veda of Susruta, dating from the sixth century. The
disease bore the distinctive name of Madhumeha or honey-urine.^
Thus the most prominent clinical feature, and one of the most widely
supported modern hypotheses concerning etiology, received their first
mention in India. But Hindu medicine failed to advance beyond this
beginning, and exerted no influence on progress elsewhere.

The Arabs are credited with nothing but passing on classical learn-
ing to modern Europe, and their two greatest physicians, Rhazes
(850-992 A.D.) and Avicenna (980-1037 A.D.) are rated by Salomon
as barren followers of Galen, whose observations serve only for evi-
dence that diabetes existed among the Arabs. But Dinguizli has
translated some passages which seem to establish an advanced posi-
tion for Avicenna. In these passages, he remarks that diabetes is
generally primary, but sometimes secondary to some other disease.
He describes the irregular appetite, the great thirst, the urine equal to
the drink, the nervous exhaustion, and the loss of sexual function and
of ability to work. In suggesting that the renal weakness is due to a
relaxed state of the nerve-plexus of the kidney, he propounds the first

* A translation by Chunder Bose is as follows: "Madhumeha is a disease which
the rich principally suffer from, and is brought on by their overindulgence in rice,
flour, and sugar. The patient feels weak and emaciated, and complains of frequent
micturition, thirst, and prostration. Ants flock round his urine. Carbuncles and
phthisis are its frequent comphcations." For other quotations, see Christie.

CHAPTER I

nervous hypothesis of diabetes. "In this disease, the liver is affected,
and its r61e of provider of heat is disturbed in consequence of the
exaggeration of organic combustions. .... The relations
between the kidney and hver become irregular, in that the kidney
attracts the humors from the liver in greater quantity than it is
able to retain them." Having thus enriched the theory of the sub-
ject with the r61e of the liver, increased metabolism, and balance
between organs, he proceeds to give the first description of diabetic
gangrene, which spreads and causes death. Such inflammations are
due to retarded circulation in the limb, or to decomposition of the
blood, which results from diminution of water in the blood. Further-
more, the urine on evaporation leaves "a residue particularly scanty,
of a sweet taste like honey, and resembling particles of bran." If
this account proves authentic, it raises Avicenna to the rank of a
clinical genius; but the second period of diabetes still begins with
WilUs, because only the latter's observation influenced the further
development of the subject. Avicenna's treatment consisted in pow-
ders of fenugreek, lupin, and wormseed, in dosage increasing up to 45
gm. daily. This seems rather suggestive of veterinary medicine, but
both Dinguizli and Robin reported patients benefited. As with so
many other methods, the digestive disturbances mentioned sufl&ci-
ently explain any benefit produced by the treatment of Avicenna.

Trincavella (1476-1568), a Venetian, observed three cases of dia-
betes. In one, the etiology was attributed to persecution and grief.
In another, the relatives are said to have demonstrated the truth of the
Galenic doctrine that diabetic urine is the unchanged drink, by fre-
quently tasting the urine and finding the taste identical with what the
patient had been drinking. Cantani suggests that the drink in this
case was sweet tea.

Amatus Lusitanus and Zacutus Lusitanus, Portuguese physicians of
the forepart of the sixteenth century, named dietary, alcoholic, and
venereal indiscretions among the causes of diabetes. The latter con-
sidered the seat of the diabetic disturbance to be not only in the
kidneys but even more in the stomach; he thus holds a transitional
position in regard to theory between Galen and RoUo.

HISTORY 7

Aureolus Philippus Theophrastus Paracelsus Bombast ab Hohen-
heim (1493-1541) broke radically away from all old dogmas, in this
as in other subjects. He performed the first chemical experiment,
and, with surprisingly accurate insight, drew from this crude observa-
tion the first chemical concept of diabetes. The experiment con-
sisted in evaporating the urine; it was found that a "measure" of
urine yielded four ounces of "salt." Paracelsus therefore afl&rmed
that diabetes is a systemic disease, characterized by the formation of
an abnormal salt in the blood. The polyuria is not due to a renal lesion,
but the salt "makes the kidneys thirsty; for thirst always comes from
salt." He was accustomed to taste the urine of patients, but for some
reason failed to discover the sweetness of diabetic urine.

Geronimo Cardano (1505-1576), an Italian, claimed that a girl of
eighteen years took seven pounds of food and drink daily and excreted
thirty-six pounds of urine, thus proving Celsus' notion that the fluid
output is greater than the intake in diabetes, the excess being suppos-
edly drawn from the air. In addition to this mistake, there is evidence
that the girl did not even have diabetes; but a step forward is repre-
sented by this first record of a case history and a chnical experiment.

Rembert Dodonaeus (1517-1586), a Dutch physician, first mentioned
chyluria in a diabetic'

Johann Baptista van Helmont (1578-1644), of Brabant, followed
the chemical theory of Paracelsus and regarded diabetes as a disease
of the blood. He was the first to record an observation of diabetic
Upemia.'

Franciscus Deleboe Sylvius (1614-1672), professor at Leyden, took
a step backward, in holding that the offending substance in the blood
in diabetes is a volatile salt.

' "Albida autem urina erat, non transi)arens, et paulo quam serum lactis
tenuior."

' "Atque in diabete, totus cruor mutatur in lotium lacteum."

II. The Second or Diagnostic Period (1675-1796).

Thomas Willis (died 1675), Sidley Professor in Oxford University,
was the first Englishman to make an important contribution to the
knowledge of diabetes. This was the simple observation that the
urine is "wonderfully sweet, as if imbued with honey or sugar."' He
did not guess that the sweetness is actually due to sugar. He held to
the theory that diabetes is a disease of the blood. The water is not
properly combined with the solid matter, so that the water escapes
through the kidneys, carrying large quantities of salts with it. Per-
Jiaps there is some disorder of the kidneys also. The resulting thick-
ening of the blood causes the excessive thirst. Urine containing so
much salt should taste salty; "but why it is wonderfully sweet like
sugar or honey, this difficulty is worthy of explanation." He thinks
it may be explained by the manner in which acids and salts alter one
another's taste. Acid salts are formed in the blood in various diseases.
Also a possible source of such acids is fermentation, as of wine and cider.
Therefore immoderate use of these liquors is a leading cause of dia-
betes. It may also be brought on by bad hygiene, worry, and nervous
aiknents. Treatment should aim to thicken the blood and supply
salts. Accordingly, milk, rice, and starchy and gummy foods are
indicated; and by Umiting a patient to a diet of milk and barley-water
boiled with bread, Wilhs became the author of the first carbohydrate
or undernutrition cure. He employed Hme-water as a beneficial form
of salt; it held a high place in diabetic therapy for well over a century,
and was the first alkali to come into general use in diabetes. Certain
other drugs owed their general adoption largely to his example, even
though he was not the first to use them. Thus, his antimony treat-
ment was in favor more than a century after his death and led to some
interesting developments, and his Dover's powder and tinctura the-
baica fastened upon the medical profession an opium habit in diabetic

' "Quasi melle aut saccharo imbutam, mire dulcescere."

8

HISTORY 9

treatment which is very difl&cult to break even at the present time.
Superficially, the sweet taste of the urine appears such a primitive and
fortuitous observation as might have fallen to the credit of anybody
in the 2000 years of European medicine from Hippocrates to Willis.
But, with due allowance for the inevitable element of chance, the above
record makes it clear that this, like most discoveries, fell to the lot of
the man whose point of view and whose methods were capable of yield-
ing discoveries. It marked a triumph of modern independent thought
and objective clinical study over subservience to authority and dogma.
It was of epoch-making importance in the history of diabetes; first,
because it established a radically new and decidedly more accurate
basis for diagnosis, which had previously depended upon polyuria and
other uncertain symptoms; and second, because it led first to the
dietary treatment of RoUo and his successors and later to the experi-
mental work of Claude Bernard and all subsequent investigators of the
normal and abnormal metaboHsm of carbohydrates. It may in some
measure be due to the stimulus given by Willis that for nearly two
centuries (viz., until Bernard and Bouchardat transferred the leader-
ship to France) the important progress in the subject of diabetes was
practically confined to Great Britain.

Thomas Sydenham (1624—1689), hailed as a second Hippocrates in
general medicine, contributed nothing of value in diabetes except a
clearer definition as a disease of metabolism. Because the nutritive
elements of the blood are not properly prepared for assimilation, they
pour out through the kidneys, and the flesh and strength melt away.'
Later h3^otheses of free versus combined sugar are here anticipated.
In treatment, Sydenham prescribed narcotics and theriak; also, "Let
the patient eat food easy of digestion, such as veal, mutton, and the
like, and abstain from all sorts of fruits and garden stuff;" but no
effective dietetic treatment grew out of this advice.

Richard Morton (died 1698) likewise regarded diabetes as "a con-
tinual flow of nutritive juice pouring out through the kidneys, which

' "Sued sanguini illati per vias urinarias crudi, et inconcocti, exitum sibi
quaerunt; tuide sensim labefactantur vires, colliquescit corpus, et quasi substantia
ejus per banc cloacam exinanitur, cum siti, ardore viscerura, lunxborum coxarum-
que intumescentia, et salivae spumosae exspuitione crebra."

10 CHAPTER I

frequently befalls intellectual persons, and drinkers of brandy and
diuretic liquors."" He was the first to note its hereditary character.
Milk, diet was a feature of his treatment. He opposed the bleeding
and purging in use among some physicians.

Richard Mead (died 1754) was the first to consider diabetes a dis-
ease of the liver, and brought supposed necropsy evidence in support
of this view. On the Continent also began a careful postmortem
search for lesions causing diabetes, but nothing of significance was
found.

Matthew Dobson (1775) completed the discovery of Willis, and
with his paper in English, the history of diabetes emerges froni Latin
into the modern languages. He first grasped the fact that the sweet
substance in diabetic urine is sugar, proving this experimentally by show-
ing that such urine was subject to alcoholic and acetic fermentation,
did not coagulate on heating or addition of a mineral acid, but on
evaporation four pounds of a patient's jirine yielded a whitish cake
weighing four ounces, two drams, and two scruples. This cake
"smelt sweet, like brown sugar, and could not be distinguished from
sugar, except that the sweetness left a slight sense of coolness on the
palate." The urine of the same patient in convalescence yielded a
less abundant dark residue which was not sweet. Dobson also was the
first to discover a sweet taste in diabetic blood serum. He therefore
concluded that the sugar contained in normal chyle is assimilated by
the body, so that the trace in normal blood is so slight that its taste is
overcome by that of the salts. In diabetes this transformation is
slowed, so that sugar accumulates in the blood. Also, the quantity
of sugar in some cases is too great to be derived entirely from the chyle,
therefore sugar must be formed by some abnormal fermentation in the
body. The diabetic loses flesh and strength because of the loss of
nutritive material in the urine, therefore he should eat as much as
possible to make up for this loss."

^^ "Continuus succi nutritii fliixus per renes decurrens, qui cogitandibus, et
vini Gallici liquorumque diureticorum potatoribus plerumque accidit."

" A prototype of the modern fallacy of replacing through the diet the calories
lost in the urine.

HISTORY 11

Thomas Cawley*^ (1788) by a careful account of a single case, earned
credit for the first example of diabetes decipiens, the first diagnosis
of diabetes by demonstration of sugar alone, and the first description
of a pancreatic lesion in a diabetic necropsy. He, however, regarded
diabetes as a disease of the kidneys.

William Cullen (1709-1790) was the first to regard diabetes as a
disease of the nervous system, comparing the polyuria with that seen
in spastic states. He also wrote: "I think I have met with one in-
stance of diabetes, in which the urine was perfectly insipid; and it
would Seem that a like observation had occurred to Dr. Martin Lister.
I am persuaded, however, that such instances are very rare, and that
the other is by much the more common and perhaps the almost uni-
versal occurrence, I judge, therefore, that the presence of such a
saccharine matter may be considered as the principal circumstance in
idiopathic diabetes." Thus, Cullen and Lister called the attention

'^ This name often appears in the literature incorrectly as Cowley. The essen-
tials of his concise report are interesting to quote verbatim.

"Allen Holford, Esq., aged thirty-four years, strong, healthy, and corpulent, ac-
customed to free living and strong corporeal exertions in the pursuit of country
amusements, in December, 1787, was seized with diabetes; but the cause of the
great degree of emaciation and debiUty which gradually came on was not dis-
covered until March 20, 1788; at which time his urine was found to be sweet,
fermentable with yeast, and two pounds, on evaporation, jdelded about five or six
ounces of sweet black extract, exactly resembling that preparation of melasses
made by confectioners for children, and vulgarly called coverlid.

"Within the above mentioned period the quantity of urine evacuated was never
observed to exceed what is usual in health, or to be disproportioned to the ingesta,
though the state of it had been frequently inquired into, and even the quantity of
liquids drank and voided measured. For these reasons the quality of it was not
suspected until it became inconceivable, considering the quantity of aliment taken
in, how such a degree of exhaustion could ensue, unless the body was drained by
the quality of what was rejected as apparently excrementitious.

"Variety of medicine, the usual consequence of inefficacy and despair, were suc-
cessively administered. Decoction of bark with vitriolic acid and alum, with
astringents and aromatics, with chalybeates, with sacc. saturni and opium, and with
cantharides, together with cold bathing in salt water, were theprincipalmeans used,
and at first had a very good effect; but soon afterwards every medicine disagreed
with the stomach, and the patient gradually sunk and died on the 18th of June."

"The pancreas was full of calculi, which were firmly impacted in its substance.
They were of various sizes, not exceeding that of a pica, white, and made up of a

12 CHAPTER I

of the medical profession to the possible existence of diabetes insipi-
dus.i' GuUen first added the adjective "mellitus" to the name of the
disease. Cullen's theory of diabetes was that of Dobson, with whom
he had discussed it. "I formerly communicated this idea to Dr.
Dobson, who adopted it, and published it; but I must confess that
the theory is beset with difficulties, which cannot at present be solved."
He gave a wholly pessimistic view of the treatment and prognosis;
he had tried the known methods on twenty diabetic patients and failed
to save any of them.

John Brown (1735-1788) conceived life as motion. Diabetes, as a
disease of weakness, should be treated by exercise, which should be
neither too slight nor too severe. But Brown's treatment was inferior
to that of his predecessor Celsus, in that abundance of food and drink
was also prescribed for strengthening.

Johann Peter Frank (1745-1821), the most renowned German phy-
sician of his time, gave the name of diabetes decipiens, or deceptive
diabetes, to the condition of glycosuria without polyuria described by

number of lesser ones, which made their surface rough, like mulberry stones; and
in all respects they appeared analogous to the calculi which we sometimes meet
with in the salivary ducts. The right extremity of the pancreas was very hard,
and appeared to be scirrhous."

"Experiment I. — A small quantity of urine, set by in a phial, spontaneously
entered into the viaous, and then into the acetous fermentation, discharging a
great quantity of mephitic gas. A white cloud formed in the center, which gradu-
ally fell to the bottom in the form of a white precipitate. In short, the whole of
this experiment corresponded with Dr. Dobson's."

"Experiment IV. — ^A small quantity of the extract put into spirit of wine neither
dissolved nor communicated any colour to it, but immediately became very hard
and brittle.

"It appears, by the last experiments, that the extract consists of sugar united
with gummous or coagulable matter, all of which ought to remain in the body for
its support, and that little of what is excrementitious passed through the kidneys
but superabimdant water, the vehicle of this nutritious matter."

^^ They did not clearly demonstrate the existence of such an entity, for Bard-
sley (mentioned by Watt, p. 14, who gives the above quotation) criticized their
findings by showing that a urine with no perceptible sweet taste might form
more or less oxalic acid when examined chemically. This formation of oxalic acid
on treatment with a mineral acid was the first chemical method for the demon-
stration of sugar in urine, and was used by RoUo and his immediate successors.

HISTORY 13

Cawley. He also established the definite division and nomenclature
of diabetes insipidus or spurius and diabetes mellitus or verus.

Francis Home diflCerentiated "watery" and "milky" diabetes." He
proved experimentally that the urine of a diabetic patient was not in
excess of the fluid in food and drink. He isolated sugar from the urine
of two patients, respectively an ounce and an ounce and a half of
sugar to the pound of urine. Addition of yeast to the urine was fol-
lowed by fermentation; the urine lost its sweetness and acquired the
taste of small beer. He failed to confirm Dobson's observation of the
sweetness of diabetic serum. He upheld Dobson and CuUen's theory
of diabetes as a defective assimilation of food. The sweet urine,
milky in some cases, was evidence to him that vegetable foods are not
properly assimilated in diabetes; the sweet chyle, which is the first
product of digestion, is not converted into ammonium salts as it nor-
mally should be. Therefore diabetes should be curable by strict meat
diet; but he was unable to make this theory succeed in practice, and
he went on to try a multitude of drugs without result. Given suffici-
ent courage or skill to build on this theory a successful practical
method, he might have been the founder of the new era of therapy.

^*The relatively frequent mention of milky urine among early writers is re-
markable. Perhaps the appearance was due to fermentation. Whether in the
absence of dietary regulation there may have been occasionally a true visible
lipuria is a possible question of interest.

III. The Third Period, or Period of Empiric Treatment
(1796-1840-50).

John Rollo, a surgeon-general of artillery in the English army,
ventured to try an entirely original method on the first case of dia-
betes that he had ever treated. "For the case I had seen at Edinburgh,
and Dobson's account, with Dr. CuUen's opinion, had prepossessed
me with the idea of the disease being a primary and pecuUar affection
of the stomach" ( (2), p. 5)." This first patient, a certain Captain
Meredith, treated in 1796, shares some of his physician's fame, not
unjustly, in view of what he went through. The treatment began
with bleeding, which is said to have made the patient feel better.
Confinement to the house was ordered, preferably to one room, with
the utmost possible quiet and avoidance of exercise. The bill of fare
was as follows: "Breakfast, I5 pints of milk and J pint of lime-water,
mixed together; and bread and butter. For noon, plain blood pud-
dings, made of blood and suet only. Dinner, game, or old meats,
which have been long kept; and as far as the stomach may bear, fat
and rancid old meats, as pork. To eat in moderation. Supper, the
same as breakfast." The skin was to be greased daily with hog's
lard, flannel worn next the skin, and an ulceration about the size of
half a crown to be maintained opposite each kidney. At first, kali
sulphuratum was ordered several times daily, but later this was ex-
changed for "hepatised ammonia" (ammonium sulphide), "a medicine
proposed by Mr. Cruikshank, who was of the opinion that it might
prove a more certain and active medicine than the other on the stom-
ach, in diminishing its action, as well as that of the system in general."
Wine of antimony and tincture of opium were to be taken at bedtime,
and "in reserve, as substances diminishing action, tobacco and fox-
glove." Captain Meredith's age was thirty-four, and his diabetes of
seven months' standing, apparently moderate in degree. He steadily

^' This rules out the statement by various authors that Rollo received his stimu-
lus from Home.

14

HISTORY 15

improved, in spite of occasional indulgence in apple pie or beer. Along
with the gain in strength and disappearance of symptoms, Rollo noted
diminution in the quantity and sweetness of the urine, in the amount
of sugar obtained on evaporation, and in the oxalic acid test. After
cessation of glycosuria, the strict diet was gradually relaxed, and it is
complimentary to RoUo's judgment that the first vegetables permitted
were cabbage, boiled onions, salad, mustard, common radish, and
horse-radish. The patient resumed his military duties. Rollo under-
took his second case, that of "a General Officer." Here the diabetes
was of three years' duration, and the patient, aged fifty-seven, re-
peatedly broke even the rather mild regimen imposed, so that he
ultimately died.

Various other matters of interest are contained in Rollo's book.
The diuretic action of sugar is clearly recognized. ((2), p. 24) : "The
serum of the blood apparently containing less saccharine matter than
the urine, may depend on the power of the kidneys in separating it
in common with the other saline matters of the blood; but proving a
new and peculiar stimulus, their action is increased, and the saccharine
matter consequently separated speedily and in proportion to its for-
mation in the stomach." (P. 37) : "A diet of animal food, as rancid as
possible, was proposed in our case, with the view of preventing the
formation of sugar in the stomach, and by that means to remove the
peculiar stimulus which supported the increased action of the kid-
neys." A number of other physicians wrote enthusiastically concern-
ing the benefits of the new method. Currie (pp. 147 and 184 of
Rollo's book, 1798) reported experiments of weighing ingesta and
egesta, weighing the patient before and after bathing, etc., to refute
the ancient error of excess of fluid output over intake. Marshall de-
scribed a necropsy showing lipemia, "chyle in the subclavian vein;"
and "there appeared to be no proper blood in the body, but instead of
it, a hquid nearly resembling well made thin chocolate. All the veins
were filled with this singular brown blood, which had a sickly, sweet-
ish, slightly sour smell (not tasted)." On page 331 is the first re-
corded observation of an important phenomenon, — a diabetic aged
twenty-five, "with the odor of decaying apples in his breath." The
letters from physicians show that diabetes was a rarity and a curiosity
to them. Dr. Monro is quoted (p. 364) in a statement of the nature of

16 CHAPTER I

diabetes, which may well bear comparison with present-day views:
"Were I to give a theory of this wonderful disease, I would say that it
arises from a defect of the animal or assimilatory process, by which the
aliment is converted into the nature of our body." RoUo's theory was
inferior to that of Dobson and Monro. He held that diabetes is a
disease of the stomach, with increase of its activity, secretion of an
abnormal gastric juice, and probably increased activity of the lac-
teals; that "the saccharine matter is formed in the stomach, and
chiefly from vegetable matter." The source of sugar was to be cut
oif by restricting the diet to animal food; but milk was provisionally
included under animal food, and, to indulge the patient, a little bread
was permitted. Also, the abnormal activity of the stomach should be
depressed, so as to check bulimia and restore the secretion of a normal
gastric juice. Therefore, drugs were chosen to produce anorexia and
nausea — ammonium sulphide, antimony, opium, digitalis, tobacco.
The use of rancid fats in the diet was for a similar purpose. Fat in-
deed was responsible for the first fasting treatment of diabetes (RoUo
(2), p. 36). "Thus Villanovanus relates that a certain man, affected
with this disease, eat pot-bread dipt in lees of oil; and that a woman in
the like case drank twice the melted fat of beef, with a like quantity
of hot oil; and that both these patients contracted so great a loathing
of food, that neither of them eat anything for five days, and so got rid
of their distempers." It so happened, therefore, that the very incor-
rectness of RoUo's theory aided in his therapeutic success. From the
results achieved with his method by himself and others, he drew the
conclusion (p. 141) that "diabetes mellitus is so far understood as to be
successfully cured."

Dupuytren and Th6nard reported good results from the RoUo diet
in France, considering it as specific for diabetes as quinine for malaria;
yet they recognized that the cure is never complete, as patients re-
lapse whenever they discontinue the diet. They investigated the
properties of diabetic urine, demonstrating that on fermentation it
yielded carbon dioxide and alcohol; this was considered to prove the
presence of sugar, but this sugar was thought to be of a peculiar kind
with little taste.

Nicolas and Gueudeville held a theory similar to that of RoUo.
They regarded diabetes as a disorder of intestinal digestion; the chyle

HISTORY 17

is normally composed of nitrogenous substances, but in diabetes it
contains imperfectly elaborated materials saccharine in character and
unsuited for the nutrition of the body.

Robert Watt (1808), a Scotchman, reported benefit from treating
diabetes with the Rollo diet, bleeding, bhstering, antimony powders,
and sometimes mercury. Both food and drink were severely restricted
in quantity. Watt's clinical ability, and the position properly belong-
ing to him in the history of this subject, may be indicated by quota-
tions from his remarkable little book." His admonitions may be
profitable to many even at the present time.

Thomas Christie (1811) first brought to European notice the fact
that diabetes was known to the ancient Hindus. He described the
frequency of diabetes in Ceylon, and his success with the Rollo treat-
ment there.

"Watt, preface: "The rapid restoration of health after venesection, blistering
and an abstemious diet in cases, where from the great prostration of strength and
excessive emaciation, a stimulating mode of treatment seemed indicated, dis-
closes views of the animal economy by no means favourable to some modern opin-
ions. It is to be feared that a dread of debility and an emaciated state of body,
from an inflammatory, not a hectic cause, have sometimes deterred practitioners
from employing depletion, and the patient has been quietly resigned to his fate.
As diabetes is so obviously aggravated by too much aliment or stimuU, and as
there is such an attendant buUmia, the first aim of the practitioner should be
to remove a portion of that food, which, since it does not nourish, must oppress
and injure the system. Animal diet accomplishes this object to a certain ex-
tent, for during its use, the quantity of ingesta is necessarily diminished, and a
partial abstinence is enforced. More might have been done if, instead of an
exclusive confinement to animal food, the quantity of ingesta were gradually
diminished, till no more were received than the digestive organs could easily
prepare, and the functions of assimilation successfully convert to the support
and nourishment of the system. Artificial depletion may, in some measure,
supersede the necessity of too strict adherence to an abstemious diet; but the end
will imdoubtedly be more easily, and effectually accomplished if the patient can
exert the requisite fortitude to resist the cravings of appetite, and to repress urgent
thirst. These indulgences increase the flame, which sooner or later consumes the
patient. We aid the cure by a diminution of the supply, and the same means pro-
tract the fatal period, or smooth the passage to the grave, when a cure is beyond
the reach of art."

Watt (p. 29 ff.) described the treatment of a laborer suffering from moderate
diabetes. The man was bled daily, the quantity of blood taken being generaUy

18 CHAPTER I

Chevreul in 1815 demonstrated that the sugar of diabetic urine is
identical with glucose.

Latham (1811) distinguished two forms of diabetes, the saccharine
and the seirous. Likewise Gregory (1825) described the differences
between diabetes mellitus and diabetes insipidus. Such observa-
tions were of importance in settling the existing doubts among the
medical profession as to the decisive import of glycosuria for the diag-
nosis of diabetes.

Pelham Warren (1813) may be mentioned as the leading English
opponent of the Rollo treatment. He regarded dietary restriction as
of merely secondary importance, and voiced the frequent objection
that patients would not adhere to such a diet. He placed chief de-
pendence on large doses of opium, by which, without dietary regula-
tion, he obtained diminution of glycosuria and polyuria. Some
authors have referred to him as the originator of opium therapy. He

fourteen or eighteen ounces, but on one day twenty-four ounces. The bleedings
were well borne, and after^ twelve days there was marked improvement. Anti-
mony powders were also used, and the patient in consequence "was very sick and
uneasy all day; had no appetite for food." Again (p. 35): "The antimonial
powders appeared to have a more decided effect. They produced very severe
sickness, vomiting, and commotion in the stomach and bowels. The night after
taking these, the urine was greatly reduced, and next day he found himseK un-
commonly weU. On repeating them, they had not such violent effects, nor was
the relief obtained so decisive. . . . Anything which produces sickness has
a temporaiy effect in relieving diabetes, by diminishing the quantity of ingesta.
The antimonial powders seemed to possess no other specific action. During the
two days he was under their influence, he vomited everything, and was not dis-
posed to take either meat or drink, hence when the supply is cut off, the excretion
must diminish of course." (P. 204) : "The loss of balance between the digestive
and assimilative organs may be produced in two ways" (underf unction of lungs or
overfunction of lacteals). (P. 205) : "In some diseases the receptive power is not
only continued but even increased, whUe the assimilative powers remain at or
below their normal level." Finally, (p. 212): "Diet. From the very nature of the
disease, abstinence becomes an indispensable part of the practice. This doctrine,
however, is often very contrary to the feelings of the patients, who are apt to urge
in their defence that nature is the best judge of what is necessary for their support.
They feel weak, they have a strong craving for food, and they can see no reason
why they should be deprived of what makes other people strong. These argu-
ments are frequently repeated, though every meal might convince them that it
has added to their burden and not to their strength."

HISTORY 19

failed to take account of the effect of opium upon appetite, and he may
be considered the founder of the erroneous belief, still widely prevalent,
that opium has an actual specific effect upon diabetes.

RoUo's treatment seems to have met with chiefly an adverse judg-
ment in Germany." It never gained general adoption by the medi-
cal profession of any country, unless perhaps England; and though
it always had eminent supporters, and more or less restriction of carbo-
hydrate continued to prevail, yet the weight of opinion and practice
even in England gradually turned against strict animal diet. The
decline in popularity may be attributed to the crudeness and imper-
fections in the method itself, the careless and faulty application of it
by most physicians, the rebellion of patients — ^who generally, sooner
or later, secretly or openly broke the intolerable dietary restrictions
and relapsed — the failure of the method to check the severest cases,
and the frequent bad results, well understood nowadays, of changing
diabetic patients suddenly from mixed diet to strict protein-fat
regimen.

Prout, though transitional in time and influenced in his later years
by Bouchardat, may be mentioned as closing this period. Naunyn
( (5), p. 388) credits him with being, in the 1820 edition of his book,
the first to restrict protein in diabetes; but such instructions (1848
edition, p. 40) were intended only to forbid overloading the stomach
at any one time, so that Front's advice was not superior to RoUo's and
far inferior to Watt's. His treatment was based on the theory (p. 38)
"that diabetes is nothing more nor less than a form of dyspepsia;
that this dyspepsia principally consists in a difficulty of assimilating
the saccharine alimentary principle." He did not approve of strict
animal diet, but gave especially green vegetables with it. He (p. 44)
introduced the use of bran bread, to be made with eggs and milk, the
bran being finely ground to avoid irritation of a sensitive intestine,^'
and washed in a cloth till the water came through clear to remove

^' Cf. unfavorable experiences reported by von Stosch, Wolff, and Horn, ref. by
Ebstein((2), p. 11).

'* Camplin (1858) stated that the use of bran for diabetic bread had been known
for a long time, but it was not highly considered. He was a diabetic treated by
Prout, and suffered diarrhea from bran bread; therefore he originated the plan of
having the bran ground very fine in a special mill.

20 CHAPTER I

starch. He limited drink as well as food. He employed bleeding,
Dover's powder, antimonials, and other drugs, but cathartics only as
needed to regulate the bowels. In thirty years of practice he saw 700
diab.etics. He considered that cold, dampness, or malaria brings on the
disease in predisposed persons. He described the frequency of phthisis
as a fatal complication, the liability to sudden death from indigestion,
travel, or exhaustion; and in particular, he was the first to mention
coma as the typical termination of diabetes, as follows: (pp. 28-29)
"The person and breath of the patient often exhale a sweetish hay-
like odour. Accompan3dng these bodily symptoms there is great de-
pression of spirits and despondency. .... The breath becomes

short, and there is more or less of cough and expectoration

The emaciation and debility now rapidly approach the maximum; the
tongue and fauces assume a dark red colour, and often become aph-
thous; the urine generally diminishes in quantity, and loses much of
its saccharine property; the feet and legs become edematous; and,
finally, after almost a total suppression of the renal secretion, the
patient becomes comatose, in which state he expires." Also (p. 61.) :
"In young children, the sudden withdrawal "of fluids, as well as the use
of opium, require caution, from the tendency of these expedients to
cause a suppression of urine, which is almost certain to terminate in
coma and death."

IV. Modern or Experimental Period.

Though this period began in the decade 1840 to 1850, the way was
prepared, as usual, by a few brilliant forerunners, who may properly
be included here.

Lavoisier" (1743-1794), who discovered the most important
properties of oxygen, substituted chemical union for the phlogiston
hypothesis, and determined that plants consist essentially of carbon,
hydrogen, and oxygen, while animals contain also nitrogen, pointed out
the relation of oxygen to the processes of life. He proved that it,
and not nitrogen, is essential for respiration. He recognized that
animal life and heat are dependent on oxidation. He performed the
first experiments concerning human respiratory metabolism, and
actually obtained correct values for the normal oxygen consumption
of man, and demonstrated the increase due to cold, work, and diges-
tion. Such an achievement is a most remarkable display of genius in
a man whose work preceded RoUo's publication, and whose career was
untimely ended by the guillotine of the French Revolution. Further
research was lacking in this line until Regnault and Reiset in 1849
conducted experiments with a respiration chamber for animals.

Tiedemanh and Gmelin (1827) in animal experiments proved that
sugar is normally formed from starch in digestion. By the fermenta-
tion test they also demonstrated sugar in the portal and systemic
blood of animals after carbohydrate feeding, but supposed it to be
absorbed through the chyle. .

Ambrosiani, also Maitland,^" by the same method discovered the
presence of fermentable sugar in the blood of diabetic patients, though
Claude Bernard criticized their results because white of egg was used
to clarify the solution. M'Gregor claimed to find sugar in the vomitus
of a diabetic who for three days had received only roast beef and water,
thus, supposedly demonstrating the origin of diabetes in an abnormal

'^ See Lusk, Chapter I.
^^ Mentioned by M'Gregor.

21

22 CHAPTER I

gastric function. He also reported the presence of sugar in diabetic
saliva and feces. Also, by fermentation, he demonstrated sugar in the
blood of a considerable number of his diabetic patients, and found
traces in the blood of normal persons during digestion of starch. Mag-
endie and von Frerichs confirmed these blood sugar findings.''^ Mean-
while Thomson had attempted the first quantitative determination,
fijiding by fermentation only 0.03 to 0.06 per cent of sugar in chicken
blood.

Other movements in science about this time must be borne in mind
in connection with the remarkable new developments in the field of
diabetes: Wohler's synthesis of urea in 1828, breaking down the sup-
posedly absolute barrier between the domains of the organic and inor-
ganic; the cell theory enunciated by Schleiden in 1838 for plants, and
by Schwann in 1839 for animals; the beginning of Virchow's work on
cellular pathology with his appointment as Privatdozent at Berlin in
1847; and meanwhile the laying of the foundations of physiological
chemistry by Liebig. In addition to the deeper problems thus thrown
open, certain chemical tests deserve notice; these were the polari-
metric determination of sugar discovered by Biot in 1833, the first
copper reduction qualitative test devised by Trommer and announced
after his death by MitscherUch in 1841, and the quantitative method
of Fehling in 1850. It is hard to overestimate the important influence
of these easy and striking sugar tests upon the development of the
theory of diabetes. Also, by furnishing the first means for the accurate
qualitative and quantitative detection of sugar even in small quanti-
ties, they had a great and immediate effect on both diagnosis and
treatment.

Claude Bernard contributed nothing directly to the treatment of
diabetes, but stands as an epoch-making figure of the new period be-
cause of the extensive physiological researches by which he not only
founded modem knowledge of carbohydrate metabolism, butjalso
clearly established animal experimentation as a method for solution of
the problems involved. His scientific career began in 1847, his first
work being the demonstration of sugar in the right-heart blood of dogs
fed exclusively on meat. This inconclusive experiment seemed then

*^ For other early literature see von Mering ( (1), p. 386).

HISTORY 23

to overthrow the prevailing doctrine that only plants and not animals
can form sugar from non-carbohydrate materials. By this and other
experiments Bernard founded the theory of sugar formation from pro-
tein, which was not to receive actual proof until some years later.
He performed the first reasonably accurate quantitative determina-
tions of blood sugar, some of his values being too high, presumably
because of injury and excitement of the animals, but other figures,
such as 0.107 per cent, being of a character now recognized as normal.
He discovered glycogen and the glycogenic function of the liver; he
considered that glycogen is formed from either the carbohydrate or
the protein of the food, and that the liver from its glycogen suppHes
sugar to the circulation in the intervals between digestion. He ob-
served sugar formation from glycogen in the liver post mortem, and
proved that the process was due to a diastatic enzyme, which was held
to be the agent of this action also during life. He discovered curare
glycosuria, and, more important, the glycosuria produced by puncture
of the floor of the fourth ventricle, giving the first experimental foun-
dation for the conception of nervous glycosuria. To Bernard, dia-
betes and piqiire glycosuria were temporary and permanent forms of
the same thing. The nervous irritation was supposed to cause
splanchnic vasodilatation and hyperemia of the liver; this produces
increased contact between liver glycogen and blood diastase, and the
resulting acceleration of glycogenolysis floods the body with sugar,
the excess of which flows away in the urine. It was thus a pure over-
production hypothesis, and the liver was in Bernard's opinion the
organ principally concerned.

Mialhe in 1845 announced the discovery of the diastase of saliva.
Apparently as an outgrowth of his diastase studies, he set up the hy-
pothesis that diabetes is a primary acidosis, that the blood of patients
has an acid reaction due to ingestion of too much acid, or to deficient
sweating and the resulting retention of acids; and he introduced a
treatment with large doses of alkali, especially sodium bicarbonate and
magnesium hydrate. Though claiming some benefits at first, he and
those repeating his attempt soon met failure. Under the tests of
Bouchardat, Griesinger, Kulz, and others, both theory and therapy
fell. Later Mialhe (3) concluded that the primary cause of diabetes
does not consist entirely in an abnormal composition of the blood, but

24 CHAPTER I

in an essential nervous disorder. The fallacious comparison between
the diabetic process and the r61e of acids in the hydrolysis of starch or
glycogen in vitro has caused such a theory to reappear in various forms
from that time to the present.

Though Bouchardat (1806-1886) read his first memoir to the Acad-
emy of Sciences in 1838, and the final edition of his book appeared in
1875, he came into prominence thrbugh important contributions in the
decade 1840 to 1850. Like Rollo and aU other founders of the dietetic
treatment, he considered diabetes a disease of digestion. According to
his theory, normal gastric juice has no action upon starch, which is di-
gested in the intestine; but in diabetes, an abnormal ferment digests
starch in the stomach, and glycosuria, polyuria, and other symptoms
result. He claimed to demonstrate the presence of diastase in the
vomitus of diabetics and its absence in that of normal persons."^
Hypertrophy of the stomach and atrophy of the pancreas in diabetic
necropsies were also held to support his theory; and he was thus
the first to suggest an influence of the pancreas in the causation
of diabetes, and the originator of the attempt to produce it by pan-
createctomy in dogs.^* For sugar determination in urine, he used
fermentation, the polariscope, and the Frommherz copper reagent.
By the fermentation method he showed the presence of sugar in dia-
betic blood, but found none in normal blood. At how low an ebb
was the Rollo treatment at this time is shown by the pleading and

'^^ Various other authors reported similar results: cf. Griesinger, pp. 41-42.

^' Some authors attribute the first pancreatectomy to Brmmer in 1686, but his
extirpation aimed only to produce hypertrophy of the duodenal glands named after
him, and involved less than half of the pancreas. Bouchardat ((2), p. 108)
ascribed to Haller (1708-1777) the observation that depancreatized dogs show
polydipsia, polyphagia, emaciation, and death. This statement has been widely
copied in the literature. But pancreatectomy to the point of diabetes was scarcely
possible at such an early datCj and as Haller apparently never published any such
work (cf. Sauerbeck), the entire myth seems to have originated in a mistake of
Bouchardat. The first attempt at total extirpation and the first idea of producing
diabetes by this means were represented in Bouchardat's publication in 1846 of
experiments undertaken with Sandras to support the pancreatic origin of diabetes.
The dogs did not survive pancreatectomy, and ligation of the pancreatic duct did
not produce diabetes. The undeveloped state of surgery therefore barred Bou-
chardat from reaping the fruits of his brilliant intellectual perception in this field.

HISTORY 25

arguments of Bouchardat ( (1), p. 10). He begs all friends of truth
to hear him; whatever be the original cause of glycosuria, diabetics,
who otherwise all die, are actually saved when his dietetic treat-
ment is used. Bouchardat in the clinical field ranks with Claude
Bernard in the experimental field. He is easily the most brilliant
clinician in the history of diabetes. He resurrected and transformed
the Rollo treatment, and almost all the modern details in diabetic
therapy date back to Bouchardat. He was first to insist on the need
of individualizing the treatment for each patient ( (2), p. 150). He
disapproved the rancid character of the fats in the Rollo diet, but
followed an intelligent principle of substituting fat and alcohol for
carbohydrate in the diet. H.e forbade milk because of its carbo-
hydrate content. He urged that patients eat as little as possible,
and masticate carefully; also (1841) he inaugurated the use of oc-
casional fast-days to control glycosuria. Subsequently he noted the
disappearance of glycosuria in some of his patients during the pri-
vations of the siege of Paris. Though the introduction of green
vegetables is credited by Prout (p. 45) to Dr. B. H. Babington, the
honor of thus successfully breaking the monotony of the Rollo diet
.properly belongs to Bouchardat.- He recommended them as furnish-
ing little sugar, a little protein and fat, but especially potassium, or-
ganic acids, and various salts. He also devised the practice of boiling
vegetables and throwing away the water, to reduce the quantity of
starch when necessary. As a similar trick ( (2), p. 217) he "torrefied"
(i.e., charred and caramelized) bread to improve its assimilation;
possibly this is the origin of the widespread medical superstition that
diabetics may have toast when other bread must be forbidden. He
invented gluten bread; this started the idea of bread substitutes,
from which sprang the bran bread of Prout and Camplin, Pavy's
almond bread, Seegen's aleuronat bread, and the numerous later
products. Bouchardat also first introduced the intelligent use of exer-
cise in the treatment of diabetes, and reported the first clinical ex-
periments proving its value. He showed that carbohydrate tolerance
is raised by outdoor exercise; and to a patient requesting bread, he
replied ( (2), p. 228) : "You shall earn your bread by the sweat of your
brow." There is a modern sound to his complaints ( (1), p. 47) of the
difficulties of having treatment efficiently carried out in hospitals, of

26 CHAPTER I

the lack of adequate variety of suitable foods, of deception by patients,
and of how, even when improved in hospital, they break diet and
relapse after returning home. He advocated ( (2), p. 330) daily test-
ing of the urine, to keep track of the tolerance and to guard against a
return of sugar without the patient's knowledge. He followed Mialhe
in giving alkalies, viz. sodium bicarbonate up to 12 to IS gm. per day,
also chalk, magnesia, citrates, tartrates, soaps, etc., also ammonium
and potassium salts; he found them often beneficial to the patients
but not curative of the glycosuria. He told a patient ( (2), p. 120):
"You have no organic disease; there is merely a functional weakness
of certain parts of your apparatus of nutrition. Restore physiological
harmony and you will attain perfect health . " He used glycerol for
sweetening purposes, and introduced both levulose and inulin as forms
of carbohydrate assimilable by diabetics, for reasons which well illus-
trate his intellectual keenness. On giving cane sugar to diabetics,
he had found only glucose excreted. Was the levulose utilized or
changed into glucose? Levulose proved under certain conditions to be
more easily destroyed in vitro than glucose. Accordingly he gave
levulose and inulin to diabetics, and found no sugar in the urine.
Therefore he recommended levulose for sweetening purposes, and
inulin-rich vegetables for the diabetic diet.

Sir Henry Marsh (Dublin, 1854) criticized the RoUodietas impossible
to follow because of the indigestion and repugnance to food resulting,
but he followed the Bouchardat plan with vegetables, and also used
exercise, warm clothing, and baths, restriction of fluid intake, Dover's
and James' powders, and alkahes (lime-water and hartshorn, recom-
mended by CoUes). He condemned bleeding, and found opium tem-
porary in effect. He noted that an attack of vomiting frequently
leads to death; also, "I have seen three cases of diabetes terminate
in fatal coma."

Fetters (1857), in the clinic of von Jaksch, investigating the peculiar
smeU noted by various authors, obtained from the urine of a coma
patient a small quantity of a liquid giving the reactions of acetone.
An extract of the limgs also jdelded acetone. He therefore attributed
the cause of coma to poisoning by acetone produced by digestive dis-
order. Kaulich distilled 700 pounds of diabetic urine, and purified
enough acetone to identify it by elementary analysis.

HISTORY 27

Trousseau condemned the Rollo diet. "I cannot too emphatically
raise my voice against the abuse of giving an exclusively animal diet
in diabetes." Intolerable loathing and impairment of health were
alleged against it. Trousseau followed Bouchardat's method, and
especially advocated exercise; but he also allowed fruits and even a
small quantity of bread, and confessed that patients in the emaciated
stage were beyond hope. He was the first to mention bronzed
diabetes.''*

Piorry of Paris, "a man who loved to turn everything upside down,"^'
brought into some prominence in 1857 a notion which was more ex-
cusable when first suggested by Chevallier in 1829. Since sugar is lost
in diabetes and is indispensable to life, it was proposed to replace the
loss by feeding sugar. Piorry gave only a very incomplete description
of one case, apparently mild, which he treated by almost complete
withdrawal of fluids, and by giving daily 125 gm. of sugar candy "and
two portions of meat." The polyuria necessarily ceased, and the
sugar excretion remained high in percentage but diminished in total
quantity. If the author's statement represents the entire diet, his
treatment was a crude carbohydrate and undernutrition cure. It had
disastrous consequences. Owen Rees and others are said to have
taken it up. Schiff — a, physiologist of some repute, an opponent of
Bernard on certain details of the glycogenic hypothesis, and a careful
investigator of nervous glycosuria, and one of those who removed the
pancreas (in birds) without discovering diabetes — also followed it, and
upon becoming diabetic, he applied this treatment to himself. Al-
though the diabetes had appeared late in life, it ran a quickly fatal
course, apparently because of the treatment.^* Naunyn ( (5), p. 383)
gives another example of injury from this treatment, as applied by a
quack. Though such a method now seems foolish, it should be noted

^* (P. SOI) : "I was struck by the almost bronzed appearance of his counte-
nance, and the blackish color of his penis." Autopsy showed a cirrhotic liver
twice the normal size.

^* Griesinger, p. 67. The quack practice of compelling patients to drink their
own urine is mentioned as something similar.

^'Naunyn ( (5), p. 388). It is interesting that Schiff (p. 128) had described a
slight alimentary glycosuria in himself and his brother, without suspecting its
warning significance.

28 CHAPTER I

that the orthodox treatment of severe cases has represented a similar
attempt to fill a sieve — the calories lost in the urkie being replaced by
fat in the diet, which merely brings the fatal end more slowly and in a
different form than does sugar.

Griesinger in 1859 published an analysis of 225 cases of diabetes;
and though only eight were his own and the others all from the litera-
ture, his contribution was valuable for chnical experiments and sound
judgment. He compiled the first evidence indicating excess in sugars
and starches as a cause of diabetes, but concluded that it could not
be the most important cause, or many more persons and some entire
races would have diabetes. He overthrew various current errors, but
somehow convinced himself in painstaking experiments that diabetics
may excrete large quantities of sugar in the sweat, as reported by
several other authors. From the negative findings in necropsies,
he regarded diabetes as generally a functional disorder. His most
notable achievement was the demonstration, in three separate experi-
ments on a single patient, of sugar excretion equalling exactly 60 per
cent of the protein of the diet. "These facts, remaining constant under
varied conditions, cannot be accidental; they seem much more to con-
tain the law of the relation in which, in this individual on exclusive
meat diet, the production and excretion of sugar stands to the quanti-
ties of ingested meat."

Frederick William Pavy" (1829-1911), in the year that he received
his doctorate (1853), visited Claude Bernard. He soon became one of
the latter's opponents on the glycogenic theory, and, in particular,
overthrew Bernard's claim that the hepatic or right-heart blood of a
fasting or meat-fed animal contains notably more sugar than the sys-
temic or portal blood. He accepted Bernard's view that diabetes is
essentially a disorder of the liver, but denied that the hver normally
supplies sugar to the circulation, and maintained that sugar is trans-
formed in passing the intestinal wall, that sugar reaching the circula-
tion as such is non-assimilable, and that the formation of any large
quantity of sugar by the liver during Ufe would make everybody
diabetic. His theories were largely incorrect, but his experimental
work was scrupulously careful and exact and still furnishes useful

^' See article by Hopkins.

HISTORY 29

information. The study of diabetes was the dominant interest of his
life; and though a clinician with a large diabetic practice, he has the
credit of perceiving that progress could come only from fundamental
physiological investigations. The flippant remark of Sir WilUam
Gull,28 "What sin has Pavy committed, or his fathers before him, that
he should be condemned to spend his life seeking for the cure of an
incurable disease?" is a compliment to Pavy rather than to its author.
Clinically, Pavy proved the transitory nature of the apparent benefit
from opium. He took a step backward by ignoring the quantity of the
diet aside from carbohydrate. He was among the first^' to make the
following observation ((1), p. 167): "Another feature of peculiarity
belonging to the complaint, is the inabihty that is experienced to ren-
der the urine alkaline by the administration of the fixed alkalies and
their vegetable salts. Although I have given the carbonate of soda to
the extent of four drachms a day; the acetate of potash, half an
ounce; the tartrate of potash and soda or Rochelles salt, six drachms,
and even an ounce; and the citrate of potash, six drachms; yet, I
have never succeeded in rendering the urine alkaline, or in any way
approaching this character."

Seegen was also prominent in the battle over the glycogenic hy-
pothesis. He laid down the principle that every prolonged glycosuria
should be considered an incipient diabetes. His therapy was retro-
grade in two points: he ignored the total quantity of protein and fat
ingested, and lie denied the value of exercise, in the belief that it was
based on a false theory.

Von Pettenkofer and Voit published the first study of the respiratory
metabolism of a diabetic patient. They made the interesting remark
that they dared not inflict much fasting on a diabetic, because of the
great hunger and the difliculty of rebuilding lost tissue. Their work
was originally supposed to show a subnormal oxygen consumption by
the diabetic. Reynoso had previously attributed diabetes to dimin-
ished respiration. Ebstein (1836-1912) devoted extensive labor to the
attempt to prove that as CO2 inhibits the diastase of saliva, pancreatic
juice, and organ extracts, so also it inhibits diastase in the living body,

="8 Cf. Editorial, J. Am. Med. Assn., 1913, Ix, 1159.

^'For earlier, less definite observations, cf. Griesinger, p. 59.

30 CHAPTER I

and that diabetes is due to abnormal diastatic activity resulting from
subnormal production of CO2 in the tissues. In treatment he advised
the usual diet, also carbonated waters. He (1) claimed priority as
being the first to point out the danger of coma when antidiabetic diet
is suddenly begun. He opposed inanition, but considered exercise
beneficial through increased CO2 production. Schnee and a few others
followed this doctrine.

Kussmaul, a pupil of von Frerichs, in 1874 gave the first detailed de-
scription of diabetic coma, distinguished it from pulmonary disease,
uremia, and other terminal processes, called attention to the char-
acteristic dyspnea, and from the physiological action of acetone ob-
served in man and animals cast doubt on acetone intoxication as the
cause of the condition.

After Bouchardat, the most powerful impetus to the rigid dietetic
treatment of diabetes came from Cantani (1837-1893). A pupil
of von Jaksch, he was at once a clinician and an enthusiastic chemist
and theorist. His preface preaches that, however great the achieve-
ments of morphologic pathology, it can show only the form, and never
the process at work; only chemistry can give the solution, and he pre-
sents his findings as a beginning in the pathology of metabolism. His
first chapter lays down the principle that metabolism is disturbed by
excess of any constituent in the diet, and if the excess is prolonged, the
disorder becomes permanent; diabetes and gout are examples. In an
analysis of 218 careful case histories, he showed that carbohydrate had
practically always predominated in the diet; but critics must observe
that Cantani practised in Rome. He believed the greater frequency
of the disease in Italy as compared with Germany and Austria to be
due to centuries of over-rich carbohydrate diet. When nervous shock
or other causes seem to bring on diabetes, he thought that the incipient
disease was generally present before. He admitted that a primary
predisposition must precede, because so many persons can live on
excessive carbohydrate diet and never develop diabetes. He con-
sidered the seat of diabetes to be in "the abdominal organs of diges-
tion, the chylopoietic glandular organs" ( (l), p. 363). Atrophy of
the pancreas present in some of his own cases and those in the litera-
ture was interpreted by him as the result and not the cause of diabetes.
He believed (p. 331) that sugar is mostly absorbed through the thoracic

HISTORY 31

duct and only a small portion enters the liver through the portal vein;
and (p. 257) quoting Kiihne's 1868 text-book of physiological chemis-
try against the glycogenic theory, he expressed surprise that a chemist
like Pavy should believe that the liver could change sugar into glyco-
gen. He thought it probable that the blood sugar in health fails to
pass into the urine because burned in the epithelial cells of the kid-
ney.'" Diabetic symptoms were attributed to the non-combustion of
sugar and its circulation in excess. He claimed to show (pp. 274r-275)
that the sugar of diabetic blood is a so called para-glucose, which is
reducing but non-polarizing and non-assimilable; the kidneys trans-
form it and excrete it in the urine as true glucose. He regarded ace-
tone formation and coma as due to the digestive disorder, and as acci-
dental in character. His treatment set an entirely new standard of
strictness; this was the essential contribution made by Cantani. He
isolated patients under lock and key, and allowed them absolutely no
food but lean meat and various fats. In the less severe cases, eggs,
liver, and shell-fish were permitted. For drink the patients received
water, plain or carbonated, and dilute alcohol for those accustomed to
Kquors, the total fluid intake being limited to one and one-half to two
and one-half liters per day. For flavoring were permitted acetic and
citric acids, and distillate of orange blossoms. Lactic acid was given
regularly as the best substitute for carbohydrate and to aid digestion;
Cantani deemed that by means of it he was enabled to keep patients
on a more rigid diet than any of his predecessors. The quantity of
protein was carefully limited; 500 gm. of cooked meat per day were
considered enough for any diabetic, and 300 to 400 gm. sufl&cient to
maintain strength. The value of vigorous muscular exercise was
recognized, and it was proved by clinical tests that glycosuria was thus
diminished or abolished without change in the diet. If the glycosuria
was not otherwise controlled, fast-days were imposed, as often as once
a week if necessary. On these days nothing was allowed but water, or
sometimes bouillon three times a day. The protocols show a sharp
drop in the glycosuria on fast-days.'^ The duration of this treatment

'" This idea has lately been supported by Reicher, by Pierce, and by Woodyatt.

'' Stokvis (1886) considered fast-days as having only experimental interest,
stating that in Cantani 's records, the glycosuria returned promptly in every case
and not one showed any clinical benefit.

32 CHAPTER I

is also a noteworthy step; the regular period was three months, and
it was extended to six or even nine months if necessary to achieve
sugar-freedom. After two months of absence of glycosuria, green
vegetables were begun; and later wine, cheese, nuts, sugar-poor fruits,
and finally small quantities of farinaceous foods were added. Notice
was taken of the different tolerance for different forms of carbohydrate
(p. 230). Glycerol'^ was found to produce a return of glycosuria in
sugar-free patients (p. 258). The urine was analyzed daily during
treatment, afterward once every week, then every two weeks. The
least trace of glycosuria (p. 229) called for one or two months of abso-
lute protein-fat diet. The patient who could return to moderate car-
bohydrate diet was considered genuinely cured. If a more generous
diet brought a return of glycosuria, it was regarded not as a relapse
but as a fresh attack, caused by the same excess in carbohydrate which
produced the diabetes in the first place. This determined insistence
upon sugar-freedom was Cantani's best contribution; but it was
marred by faults which have persisted since, namely, the high calory
fat diet, the beUef (p. 231) that gain in weight is one of the most
important benefits, and (p. 386) that a slight glycosuria is preferable
to undernutrition. Regarding his failures, Cantani believed (p. 356)
that as long as the pancreas alone, or perhaps the stomach alone, is
diseased, the diabetes is curable in all cases, but after the liver is in-
volved a cure is impossible. He acted (pp. 369-370) on the theory of
sparing a weakened organ. He held the modern view that diabetes
is a unit, and that the varying cases represent different degrees or
stages, not different diseases. He distinguished two groups: cases in
which sugar disappears on meat diet, and those in which it does not dis-
appear. He judged that the lowered temperature and the slowed
respiration were evidence of a diminished metabolism in diabetes. He
thought (p. 203) that diabetes is better borne by fat than by thin people
because of their lower metabolism, and that the greater severity of dia-
betes in young persons and children is explained by the higher metab-
olism. The diminution of glycosuria on fasting was held (p. 190)

^^ Glycerol in the treatment of diabetes was first used by Basham {Lancet,
January, 1854). It was especially advocated by Schultzen (Bed. klin. Woch.,
1872, No. 35) on the basis of an erroneous chemical theory. Cf. Naunyn ( (5), p.
441).

msTOEY 33

to prove that the diabetic's own tissues are not convertible into sugar,
though the glycosuria on meat diet shows that sugar can be formed from
ingested protein. The description (p. 302) of a case of cerebral tumor,
causing paralysis of the optic and oculomotor nerves, with poljTiria
and 3 per cent glycosuria, which cleared up after several months, while
the tumor progressed and caused death, may now receive probable
interpretation at the first mention of h5^ophyseal diabetes. The
infectious nature of tuberculosis being unknown, the development of
pulmonary tuberculosis in a diabetic was to Cantani (pp. 113, 233) a
sign that the glycosuria could never be abolished, that the breakdown
in metabolism was hopeless, and death inevitable.

The authors who described gross lesions of the pancreas in diabetic
necropsies are named by Bouchard ( (1), p. 171) as follows: Cawley,
Elliotson, Bright, Bouchardat, Griesinger, Hartsen, Fles, von Reck-
linghausen, von Frerichs,Klebs, Harnack, Kuss, Cantani, Silver, Fried-
reich, Haas, Lecorche, Lancereaux.^' Zimmer in 1867 supposed that
carbohydrates are normally split to lactic acid in the intestine, but in
the absence of pancreatic juice the process stops at the stage of glucose,
with resulting glycosuria; but later he considered diabetes as a defect
of muscular metabolism. Popper (1868) assumed that diabetes is due
to lack of pancreatic juice, causing disturbance in fat digestion and
secondarily in glycogen storage in the liver. Lancereaux, a pupil of
Claude Bernard, described a form of diabetes characterized by sudden
onset, marked emaciation, polyphagia and polydipsia, characteristic
feces, and early death. He correctly interpreted this complex as
evidence of a pancreatic lesion. Hirschfeld later described similar
cases. But Lancereaux and his pupil Lapierre proceeded to assume
that all diabetes with emaciation is due to a gross pancreatic
lesion; to this diabete maigre or pancreatic diabetes they opposed the
type of diabete gras or fat diabetes, supposedly not pancreatic in ori-
gin. They also added later a "constitutional" or "arthritic" diabetes
and a "nervous" diabetes. This classification has been generally dis-
credited but still persists to some extent in France.

Baumel was the first to set up the hypothesis that all diabetes is

''Other literature is given by Sauerbeck, Rosenberger (p. 206), and Allen,
( (1), Chapter 21).

34 CHAPTER I

pancreatic in origin. When no gross or microscopic alterations could
be found, he assumed the presence of a nervous or circulatory disturb-
ance. Lack of pancreatic diastase was imagined to be the essential
factor, and the inhibition of secretion of pancreatic juice by stimula-
tion of the central end of the vagus was considered illustrative of
what might occur in diabetes of functional origin.

Bouchard followed Lancereaux in regarding diabetes with emacia-
tion as pancreatic in source. He upheld the doctrine of diminished
utilization as opposed to Bernard's view of simple overproduction of
sugar, and he classified diabetes among the diseases due to retardation
of metabolism.

Friedrich Theodor von Frerichs (1813-1885) published a work of
careful objective description, free from theories and preconceptions,
based on an experience of 400 cases and 55 necropsies. His preface
' states that he began with the exact science chemistry, passed thence to
physiology, and thence to the clinic, and writes now in the autumn of
life to present the fruits of nearly forty years' experience. The thor-
ough study and analysis of his cases, clinically, chemically, and patho-
logically, constitute the author's chief merit in extending the knowl-
edge of diabetes. He distinguished three forms of sudden diabetic
death; viz., cardiac failure, collapse, and the Kussmaul coma. To-
day it seems probable that all three are manifestations of acidosis.
By clinical experiments he made the acetone intoxication theory im-
probable. Ehrlich, with von Frerichs, investigated the glycogen in
'diabetes, not only post mortem but by liver puncture during life.
Ehrlich likewise discovered the so called glycogenic degeneration of
the renal tubules in diabetes.

Richard Schmitz of Neuenahr was the first to give conclusive dem-
onstration of complete recovery in a few cases of diabetes. Also,
among his 2320 cases he observed 26 in which the diabetes, in ab-
sence of any other discoverable cause, seemed so definitely to come
on after close association with another diabetic (through marriage or
otherwise) as to suggest an infectious transmission. Senator, Oppler
and C. Kiilz, and others have made it reasonably certain that such
cases represent mere coincidence.

Rudolph Eduard Kiilz (1845-1895) was a similar and even more
notable example of a painstaking, unbiased investigator. To him

HISTORY 35

diabetes was a mystery, toward the solution of which theorizing was
futile and only the gathering of the most complete and exact data
possible could be valuable.'^ In journal articles Kiilz published many
laboratory investigations, especially concerning glycogen. Also,
he discovered the oxybutyric acid in diabetic urine simultaneously
with Minkowski, and was first to observe it to be levorotatory. His
clinical experience of twenty-five years covered 1 100 carefully studied
cases of diabetes, of which 711 were chosen for publication. Probably
no other man ever did so much to clarify the subject by proving all
things and holding fast that which was good. His experiments were
the last which finally ended the error of excess of fluid output over
intake in diabetes. He found sugar absent from the sweat. He
showed the uselessness of lactic acid and the harmfulness of glycerol.
He proved the absolutely negative effects of various drugs, notably
sodium bicarbonate and arsenic, for diminishing glycosuria, aside from
the illness and digestive upsets produced; this lesson of KUlz con-
cerning Fowler's solution still needs to be learned by many today.
He demonstrated with exactness that Carlsbad water has no effect
upon diabetes. Although no valid evidence has ever shown that any
kind of water anj^where has specific influence upon diabetes, this
superstition is still so prevalent among both physicians and patients
that diabetics continue to flock by thousands to mineral springs like
pilgrims to medieval shrines. Kiilz disapproved of the methods of
Bouchardat, who jumped at truths without pausing to prove them;
and much of his constructive work actually consisted in establishing
on a substantial basis the suggestions of the brilliant Frenchman. He
tested the tolerance of many patients for many forms of carbohydrate,
finding ( (2), p. 528) that the assimilation is better for green vege-
tables than for the equivalent of starch in other forms; and that lac-
tose, levulose, and even cane sugar are often better borne than glu-
cose, but results are variable and levulose is often harmful and utilized
no better than starch. He was unable to formulate any fixed rule
whether glycosuria is increased by alcohol or not. By careful com-

^* Preface to "Beitrage:" "Main Bestreben ging vor Allem dahin, moglichst
exacte Beobachtungen zu liefern. In wieweit mir dies gelungen ist, in wie weit
diese Untersuchungen geeignet sind, unsere Kenntnisse von diesem in vieler
Beziehung noch so rathselhaften Leiden zu erweitern, mag die Kritik entscheiden."

36 CHAPTER I

parison between periods of days of rest and corresponding periods
with exercise, he reached the conclusion that e!xercise is beneficial in
strong patients with mild diabetes; in severe diabetes, where sugar
is excreted on carbohydrate-free diet, exercise may diminish glyco-
suria, sometimes only transitorily, or it may have no effect; and
in weak individuals with severe diabetes, there was no benefit
from exercise.'^ The great experience of Ktilz was probably the most
powerful factor in establishing the modern view of the unity of dia-
betes. His cases were classified in three groups; first, a mild group,
becoming sugar-free on strict diet; second, a "mixed" or intermediate
group; and third, the group of severe cases, with glycosuria continu-
ing on restricted diet. The numerous careful case records showed
such an abundance of gradations and transitions between these groups,
from the mildest to the most severe, that fixed distinctions between
types of diabetes were shown to be impossible. Kiilz made no use of
undernutrition or fasting. He treated severe cases by gradual with-
drawal of carbohydrate to avoid coma, reduced protein not below 110
gm. daily, and was one of the first to calculate diets according to the
caloric requirement. He was the first to introduce the practice of
systematically testing the carbohydrate tolerance of each patient.
Rumpf" claims as the greatest merit of the Kiilz system the inaugu-
ration of individually planned diets instead of indiscriminating general
rules. Notwithstanding the universal adoption of this plan by special-
ists and the better informed physicians, it is a regrettable fact that
the majority of the profession have not yet come up to the standard of
Kiilz, and the majority of diabetics still receive treatment by means of
printed hsts of "allowed" and "forbidden" foods. Kulz founded a
numerous and influential school. Of the three editors of his posthu-
mous work, Aldehoff is known for various clinical and experimental
studies, Sandmeyer chiefly for the diabetes produced in dogs by pan-
creatic atrophy, and Rumpf as a prominent clinician, who made early
studies of dextrose-nitrogen ratios in human patients (1, 2, 3), and

^' This was not only the most thorough investigation of exercise in human dia-
betes, but also an important independent discovery, for Kiilz did not know of any
previous use of exercise till after completion of his experiments.

'« Preface to Kiilz (2).

HISTORY 37

first (3) warned against loss of body fluid as an important factor in
bringing on coma.

Joseph Friedrich von Mering (1849-1908) was trained under von
Frerichs and Hoppe-Seyler. Though a clinician of high standing, his
fame rests upon his numerous experimental works, among which may
be mentioned his metabolism studies with Zuntz, the discovery (1886)
of phloridzin glycosuria, and the discovery with Minkowski (1889)
of pancreatic diabetes in dogs.

Bernhard Naunyn (born 1839) was the pupil of Lieberkiihn, Reich-
ert, and von Frerichs. Though the author of a number of researches,
they include no important discovery. His position as the foremost
diabetic authority of the time rests upon his influence for the advance-
ment of both clinical and experimental knowledge; upon his judgment,
his teaching, and his pupils; upon the fact that from his great Strass-
burg school have come the soundest theories, the most fruitful inves-
tigations, and the most effective treatment. In birth, it is to be noted
that Naunyn preceded Kiilz, and was only two years younger than
Cantani. He came into this field in the pioneer period when the
principle of dietetic management was generally recognized, but the
average practice, especially in regard to severe cases, was still a mass
1 of ignorance and inefficiency. As late as 1886, Naunyn (1) stood as
the champion of strict carbohydrate-free diet in a German medical
congress where most of the speakers opposed it. As one of the few
early German followers of the Cantani system, he maintained its
feasibility and ultimate benefit, and locked patients in their rooms for
five months when necessary for sugar-freedom. With experience, he
gradually introduced modifications, until the rigid and inhuman
method, which a majority of physicians and patients would never
adopt, became a rational individualized treatment, with a diet reckoned
according to the tolerance and caloric requirements of each patient.
The work of various pupils requires mention in this connection. Im-
portant investigations of metabolism established the basis for this
treatment, the inost notable being that of Weintraud, who proved that,
instead of having an increased food requirement, diabetics could main-
tain equilibrium of weight and nitrogen on a diet as low as or a little
lower than the normal. Minkowski discovered with von Mering the

38 CHAPTER I

diabetes following total pancreatectomy in dogs," and established
the doctrine of the internal secretion of the pancreas, as well as the
first clear conception of a dextrose-nitrogen ratio. After the early
acetone investigations and Gerhardt's discovery of the ferric chloride
reaction had failed to reveal the cause of coma, the Naunyn school
accomplished almost the entire development of the subject of clinical
acidosis in the following sequence. Hallervorden (1880) discovered
the high ammonia excretion, confirming an earlier discredited observa-
ton of Boussingault. Stadelmann (1883) established the presence in
the urine of considerable quantities of a non-volatile acid supposed to
be a-crotonic, correlated the condition with Walter's previous acid
intoxication experiments, and theoretically suggested the treatment
with intravenous alkali infusions. Minkowski proved the excreted
acid to be /S-oxybutyric, and demonstrated the presence of this acid
in the blood and a diminished carbon dioxide content of the blood.
He, also Naunyn and Magnus-Levy, applied the alkali therapy in
practice, and the latter carried out chemical and metabolism studies
which made him the recognized authority in this field. Naunyn intro-
duced the word acidosis, saying in definition ( (4), p. 15): "With this
name I designate the formation of /8-oxybutyric acid in metabolism."
The Naunyn school have consistently maintained that this acidosis
is an acid intoxication in the sense of Walter's experiments. They
demonstrated striking temporary benefits from the alkali therapy,
particularly in diminishing the danger of the change from mixed to
carbohydrate-free diet; but the practical results were never equal to
the theoretical expectations. With Naunyn, also, acidosis became
the principal criterion of severity for the clinical classification of cases.
As regards other theories, the Naunyn school have upheld the deficient
utilization as opposed to the simple overproduction of sugar in dia-
betes. They have clearly recognized the necessary distinction be-

" This is commonly supposed to have been an intentional following up of the
observations of Cawley, Bouchardat, and others. But according to Dr. A. E.
Taylor (personal conmumication) the epoch-making discovery was accidental.
Dogs depancreatized for another purpose were in a courtyard with other dogs.
Naunyn, perhaps mindful of the part played by insects in the history of diabetes,
asked, "Have you tested the urine for sugar?" "No." "Doit. For where these
dogs pass urine, the flies settle."

HISTORY 39

tween diabetes and non-diabetic glycosurias." Naunyn was next
after Klemperer to recognize clinical renal glycosuria. Though
observing that "the course of the disease is as variable as can be
conceived," he nevertheless upholds the essential unity of diabetes,
finding in heredity a link which often connects cases of the most varied
types. In regard to the etiology, he considers that "it is certain that
disease of. the nervous system and of the pancreas can produce dia-
betes;" other causes seem more doubtful. The nervous disorder
supposedly acts indirectly by setting up a functional disturbance in
the pancreas or other organs directly concerned. Underlying every-;
thing in most cases is, in his opinion, the diabetic "Anlage" or inherited;
constitutional predisposition. Naunyn has particularly supported;
the conception of diabetes as a functional deficiency, to be treated by
sparing the weakened function. He wisely emphasized the impor-
tance ( (5), p. 391) of doing this at as early a stage as possible, before
the tolerance has been damaged and the glycosuria has become "ha-
bitual." His plan of treatment is to withdraw carbohydrate gradually,
giving large doses of sodium bicarbonate in cases with acidosis as ii,
further precaution against coma. A brief increase of the ferric chloride ;
reaction is not allowed to interfere with the program. When the
glycosuria is successfully cleared up, the aim ( (5), p. 396) is if possible
to place the patient on a Rubner diet, representing 35 to 40 calories ;
per kilogram of body weight and about 125 gm. protein (pp. 407-.
408), carbohydrate being gradually (p. 415) added and then kept (p.,
416) at a figure safely below the tested tolerance. The views con-,
cerning exercise (p. 432) agree with those of previous authors; brisk
walking, etc., is found beneficial; but overexertion is harmful, especi-
ally in severe cases; and some patients seem to do best on a rest cure.
When sugar-freedom is not attained on simple withdrawal of carbo-
hydrate, protein may be reduced as low as 40 to 50 gm. daily ( (4), p.
22) and the calories also diminished, since ( (4), p. 22; (5), p. 397)

''Magnus-Levy {(2), p. 8), concerning pancreas-diabetes: "Dieser Diabetes
ist der einzige experimentelle, der tatsachlich als Diabetes zu bezeichnen ist."
Naunyn ( (2), p. 3130) : "Einen Diabetes melitus haben die Experimentatoren vor
Minkowski und von Mering nie erzeugt . D er sogenannte Kurare, der Kohlenoxyd,
etc., der Stichdiabetes und selbst der Meringsche Phloridzindiabetes, sie alle tra-
gen diesen Namen mit Unrecht."

40 CHAPTER I

diabetics may remain in equilibrium on as little as 25 to 30 calories
per kilogram. When necessary as a final resort, temporary under-
nutrition may be employed ( (S), pp. 392, 409) ; but prolonged under-
nutrition or the loss of more than 2 kilos weight should be avoided
( (4), p. 15). Loss of weight continuing over the third week of treat-
ment requires adding carbohydrate and abandoning the attempt to
stop glycosuria ( (5), p. 414). Occasional fast-days are advised if
necessary ( (5), p. 409), but only when previous treatment has reduced
the glycosuria below 1 per cent; otherwise their effect is indecisive
( (5), p. 426). It is stated ( (5), p. 425) that such fast-days are prac-
ticable for even the severest cases, and heavy acidosis is not a contra-
indication (p. 426); the ferric chloride reaction may diminish on a
fast-day (p. 414). Naunyn has not stated what hmitations apply to
the use of such occasional fast-days, but Magnus-Levy ( (2), p. 67)
stipulates that they must never be more frequent than one in eight or
ten days, and in very thin patients must be avoided altogether. Fast-
ing is nowhere recommended as a treatment for coma by Naunyn.
On the contrary, when restriction of diet produces really threatening
symptoms, his plan is to add carbohydrate and give up the attempt to
abolish glycosuria '( (2), p. 3144; (5), p. 414). Even the persistence
of a very heavy ferric chloride reaction longer than two or three days
is a signal for adding carbohydrate (p. 425). The treatment for im-
pending coma consists in maximal doses of bicarbonate and the free
use of carbohydrates, especially milk ( (4), p. 28; (5), pp. 350, 351;
also Magnus-Levy, (2), p. 77). Naunyn had some conception of
limiting the total metaboUsm ( (4), p. 14), but meant by it only a bare
maintenance diet, or the sUght and temporary undernutrition men-
tioned above. Naunyn ( (4), p. 13) states that fat does not appreci-
ably increase glycosuria; elsewhere ( (6), p. 741) that in very severe
cases it may slightly increase glycosuria; Magnus-Levy ( (2), p. 21)
that it never gives rise to glycosuria. Like others, Naunyn considers
that fat is the chief food for the diabetic ( (5), p. 449) ; that the intro-
duction of fat is the most important art in diabetic cookery ( (6) , p. 741) .
He uses it to complete the full number of calories when other foods
are restricted ( (5), pp. 408, 447); this apphes even to the severest
cases on carbohydrate-free diet with strict limitation of protein, where
accordingly much fat is given (p. 424) ; his principal care is that the

HISTORY 41

patient shall take enough of it (p. 395) ; the only reason for limiting
the quantity is the danger of indigestion (pp. 395, 424), except when
coma impends, in which case fats are replaced by carbohydrates, and
butter is especially shunned because of its content of lower fatty,
acids (p. 350). Even when sugar-freedom is attainable, certain cases
are believed to show an inherent progressive downward tendency
( (2), pp. 3135-3136; (5), p. 390). Concerning patients emaciated
down to 50 kilograms, with heavy ferric chloride reaction and the
usual accompaniments, it is said (p. 425) : "In the face of these great
difficulties and dangers, which accompany the energetic management
of these very severe cases, the prospects of being successful in per-
manently removing glycosuria are in general not very great, and usually
one will be content with a limitation of it which suffices to bring the
patient into nutritive equilibrium, that is, down to 60 to 80 gm. sugar
in 24 hours."

Lenne of Neuenahr is known chiefly for his advocacy of low
protein diet. His plan is to reduce the nitrogen intake until the out-
put falls to his so called "normal" figure; viz., 0.37 gm. urea or 1.1 gm.
absorbed protein per kilogram of body weight (about 1.3 gm. per kilo
in the diet). Carbohydrate is also limited, but the protein restriction
is considered more important. He classifies cases into four groups:
those in which (1) the glycosuria ceases on diminution of protein
without diminution of carbohydrate and the protein requirement
falls to 1.1 gm. per kilo; (2) this result is achieved only by reducing
carbohydrate as well as protein ; (3) limitation of protein and carbo-
hydrate stops glycosuria but the protein requirement never falls to
1.1 gm. per kilo; (4) glycosuria continues and nitrogen remains high
in spite of complete withdrawal of carbohydrate and strict limitation
of protein. He believes in simple overproduction of sugar without
impairment of utilization as the explanation of diabetes, and in the
correlated doctrine of sugar formation from fat. He states ( (1), p.
82) that it is not necessary to assign any upper limit for fat, since
appetite and digestion set the limit; later (2) he speaks in favor of
fat restriction, but only in the sense that the diet should be adequate
but not excessive. He does not limit fat even for the sake of acidosis,
since he disbelieves in the acid intoxication theory of coma, and cites
( (3), pp. 252-253) the example of a patient whose urine became free

42 CHAPTER I

from diacetic acid on carbohydrate abstinence, insufficient protein,
and excess of fat. He insists on abolishing glycosuria and hyper-
glycemia if possible, and opposes ( (l), p. 74) von Noorden's opinion
that some diabetics, especially the elderly, can be indulged in eating
as long as sugar is liot excreted above 20 gm. daily. Nevertheless he
refuses (p. 83) to prolong absolute carbohydrate-free diet for a week or
over. For stubborn glycosuria he has used fast-days, but prefers to
avoid any complete abstinence. His protocols show the benefits of
protein reduction, but also indicate the failure of the method in numer-
ous cases of only moderate severity.

It is desirable at this point to introduce a digression, for the purpose
of considering the so called "carbohydrate cures" as a group.

It will be observed that carbohydrate has been the touchstone of diabetic
therapy since the time of Rollo. All the orthodox theories have agreed in holding
it as the one offending substance, and a large proportion of physicians today still
conceive of dietotherapy as limited to prescribing a list of carbohydrate-poor
foods. On the other hand, the vast majority of diabetic patients have (following
or defying advice) never undergone rigid deprivation of carbohydrate for any long
time, the specialists of highest repute have granted it in the later stages of the more
severe cases, and there has grown up a line of treatment characterized by diets
heavy in carbohydrate.

The milk diet is historically first. According to Stokvis, milk was recommended
for diabetes by almost all authors in the eighteenth century. The Karell cure, pub-
lished in 1866 and still well known in the treatment of obesity and other conditions,
was a diet limited strictly to 60 to 200 cc. of skim milk four times daily. Rich-
ardson credits "Dr. Smart of Edinburgh" with priority in the use of a formal
"milk cure" in diabetes. A skim milk treatment was advocated by Donkin (1869)
on the claim that it was pleasanter than the Bouchardat plan and also more effec-
tive, as casein is better assimilated than other proteins, and lactose than other
forms of carbohydrate. Balfour, Oettinger, Winternitz and Strasser, Maurel,
Landouzy and Cottet, and numerous others championed the milk treatment, but
Kiilz, von Frerichs, and most authorities condemned it. Strasser advised three
days of milk, then three days of strict diet, and so on alternately — a schedule
which might rank high among carbohydrate "cures."

Prasad asserts that in India a diet chiefly of milk permits mildly diabetic patients
to live fifteen or twenty years. Naunyn considers that it is hard to get along with-
out milk in treating diabetes, and that milk "cures" are often beneficial. He and
his followers have used it as the principal means to ward off acidosis. Guelpa's
use of milk is mentioned later. Recently (1915) Farges has taken up the original
belief concerning milk, holding that not only is lactose perfectly assimilated in mild
diabetes, but that it actually improves the tolerance for other carbohydrates.

HISTORY 43

Sour milk and its commercial preparations have been used to some extent, but
according to von Noorden ( (1), p. 315) only 10 to IS per cent of the sugar is de-
stroyed in the natural curdling, and souring beyond this point makes the taste too
unpleasant for use; he therefore rates sour milk as neither bettfer nor worse than
sweet milk. The status of the typical milk cure as a form of undernutrition treat-
ment is universally recognized.

Second chronologically was the treatment of von During of Amsterdam, often
incorrectly styled the "rice cure." The first edition of this author's book appeared
in 1868, the fifth edition in 1905. He limited his patients to three or four meals
daUy, representing a total of 80 to 120 gm. of any cereal (frequently rice, least often
oatmeal because of its tendency to ferment), up to 250 gm. meat, moderate quan-
tities of stewed fruits, and small allowances of stale bread, milk, and wine. His
general position was a protest against overeating and luxurious living, and a "back
to nature" attempt in food, exercise, and general hygiene. He was a pioneer in
sanitarium discipline and restriction of the total diet. One interesting trick was
his use of ice and ice-water to combat polyphagia. He was a zealot in his beliefs,
but frankly acknowledged numerous failures. His method may be interpreted as
a mixed ration rather low in protein and calories, not infrequently proving prefer-
able to the protein-fat excess of which his earlier contemporaries were signally
guilty.

Dujardin-Beaumetz (1889) first recommended potatoes for diabetics in quanti-
ties below 100 gm., because they contained less carbohydrate than the usual gluten
bread. Mosse (first publication 1898) believed potatoes to be far superior to other
forms of carbohydrate for assimilation in diabetes, and attributed the supposed
virtue to their content of potassium, and perhaps also of organic acids, traces of
manganese, or oxidases. He gave as much as 1500 gm., or in polyphagia 3000
gm., not as occasional "cures" but as regular additions to the daily diet. His
records and graphic charts of comparisons between potatoes and bread reveal in
many instances a much smaller quantity of carbohydrate in the potato diets; in
other cases the quantity of carbohydrate was kept equal, but it is doubtful if
patients taking such large quantities of potatoes would eat as much of other kinds
of food as when taking bread. The alleged advantage of potatoes is thus readily
explained. Also the treatment was very bad throughout, for though the cases were
mild, there was no pretense of stopping glycosuria, which was high even in the cases
showing the imagined benefit. The treatment thus poorly founded gained wide-
spread adoption only in France. Rathery refers to the numerous patients there
who complain of glycosuria uncontrollable by strict diet, when inquiry shows that
they are consuming potatoes liberally in the belief that they are harmless and
beneficial. He finds it necessary to point out the smaller percentage of starch in
them as compared with bread or cereals. Labbe, by testing a series of mildly
diabetic patients with allowances slightly above their tolerance, composed a list of
carbohydrates in descending order of assimilation, as follows: potato, oatmeal,
macaroni, chestnuts, rice, beans, lentils, peas, milk, bread, sugars. Linossier,

44 CHAPTER I

discussing certain of these papers, properly called attention to the lower protein
and calories of the potato diets. The facts concerning potatoes are fully explained
by their relatively low food value, in that they carry little protein or fat and only a
fraction of the carbohydrate percentage of bread or cereals, while their bulkiness
tends to diminish the consumption of other foods. They are a higher homologue
of the green vegetables, and may be used correspondingly in the milder grades of
diabetes.

Von Noorden made the chance observation that certain patients showed marked
improvement in their diabetes, even to cessation of glycosuria, when placed be-
cause of digestive disturbances on a diet of oatmeal gruel. It is probable that such
rations were rather low in protein and calories. In 1902 he announced his formal
"oat-cure." Though there were ahready facts in the literature to indicate the true,
explanation, the diminution or disappearance of glycosuria on change from strict
to carbohydrate-rich diet impressed von Noorden and the contemporary medical
World as an astounding and mysterious phenomenon. Naunyn held a skeptical
attitude throughout . He favored the untenable hypothesis of intestinal fermenta-
tion supported by his pupil Lipetz, but he also (4A) early classed all carbohydrate
"cures" together and declared that the essential benefit lay in undernutrition.
Kolisch's correct suggestion of the importance of a low .protein intake was sup-
posedly disproved by the incorporation of eggs and vegetable protein in the oat
diet. Falta and others employed smaller quantities than the established 250 gm.
of oatmeal; but none perceived that the value of the "cure" diminished as the
quantities of foods were increased. The therapeutic endeavor was to make up a
full Voit diet to avoid undernutrition, depending on the supposed virtues of oat-
meal and special proteins to achieve assimilation. DiflFerences in the manner of
cooking, and even distinctions between brands of oatmeal, were asserted and ac-
cepted. The experimental goal was to discover the reason for the superiority of
oatmeal over other carbohydrates, and thus much fruitless labor was spent upon
oat extracts, digestion, renal permeability, and intestinal bacteriology. Thus the
entire clinical and experimental development of von Noorden's primary observa-
tion followed mistaken lines. Blum in 1911 attacked the foundation of the error,
by comparative tests showing the equal assimilation of oatmeal and other carbo-
hydrates when administered to diabetic patients imder identical conditions. He
likewise overthrew the perplexing claim that the severe cases are the ones that
assimilate oatmeal best; and it is now generally recognized (cf. Magnus-Levy (2),
p. 70) that cases doing well on carbohydrate "cures" are essentially mild even
though they may have appeared severe. Also in 1911, Klemperer showed that
even sugar behaves similarly when given in divided doses. The von Noorden
school has maintained, with diminishing force, that oatmeal possesses some degree
of superiority, and has arranged a scale of assimilability, in which bananas and
barley stand next to oatmeal, and wheat and rice are at the lower end. The litera-
ture up to 1913 permitted no positive conclusion. Minkowski (4) , in a sweeping crit-
icism of the Vienna doctrines, acknowledged the benefits of the oat cure. Magnus-

HISTORY 45

Levy added his experience in support of the relatively better assimilation of oat
starch. It has since become clear that the mixed or indecisive clinical observations
of von Noorden, Lampe," Werbitzki, Piskator, Richartz, Weiland, and other
authors previously referred to furnish no sound evidence of any peculiar assimila-
bility of oatmeal. On the contrary, accurate.comparative tests by Petersen, Wolff,
and Falta have fuUy confirmed Blum's position. Jastrowitz found complete simi-
larity between oats and wheat in experiments on totally and partially depan-
creatized dogs. Csonka lately proved the equal and complete elimination of the
carbohydrate of wheat and oats as glucose by phloridzinized dogs. The absence
of any specific ease of assimilation of oatmeal by human patients has been demon-
strated in the blood sugar investigations of Schirokauer, Severin, Lamp6 and
Strassner, Wolf and Gutmann, and Menke, and in the studies of respiratory
metabolism by Schilling, Roily, Roth, Joslin (2), and Allen and DuBois.

The buckwheat (Alvord), raisin, and other sporadic "cures" require no special
discussion. All the early carbohydrate treatments laid stress on the restriction to
only one form of starch, but the benefit of such limitation was always incompre-
hensible and is now recognized as imaginary. The later recommendations offer
greater variety. Labbe has introduced a "dry legume cure," with a diet of 300
gm. beans (including lima, soy, or other varieties), peas, or lentils, 150 gm. butter,
3 to 6 eggs, 3 to 6 aleuronat or gluten cakes, green vegetables, and wine. The
main thing avoided is meat. Falta, having renounced his old allegiance, now
uses "mixed cures" planned after the oat cure except that monotony is avoided by
means of alternation of all sorts of carbohydrate foods, with addition of green
vegetables.

The rationale of the carbohydrate "cures" appeared mysterious when diabetes
was regarded as a deficiency of carbohydrate assimilation, but becomes clear with
the imderstanding of diabetes as a general disorder of nutrition. Most of the diets
represented some degree of undernutrition. In the oat cure, this was attained by
the preceding and following vegetable or fast-days, adopted from Bouchardat,
Cantani, and Naunyn. Temporary relief from the overload of protein and fat
diet was afforded by the substitution of an excess of carbohydrate. The experi-
ence showed that the latter is, at least for short periods, often less injurious and
dangerous than the former. The successful results demonstrated the surprisingly
high tolerance still retained in a large proportion of diabetic cases heretofore
classed as severe. The invariable failure encountered in truly severe cases fol-
lows as a simple corollary to the defim'tion, since the nature of severe diabetes
involves inability to metabolize such quantities of carbohydrate, protein, and fat.

Aside from the carbohydrate "cures," there have long been practi-
tioners of higher and lower degree who have upheld the opposite
of Rollo's animal diet, namely, a pure vegetarian diet. Harley em-
ployed it for cases of a certain type. Kolisch may be mentioned as
the principal champion of this system. He argues that diabetes does

46 CHAPTER I

not consist in a lowered tolerance for carbohydrate, because a small
quantity of carbohydrate often causes less glycosuria than a large
quantity of protein. He regards the disorder as an overproduction of
sugar, derived from unknown compounds in the tissues. The improve-
ment of tolerance on carbohydrate-free diet, also the cessation of
glycosuria in cachexia observed by Cantani and Naunyn, are explained
as due to impoverishment in sugar-forming material. Food, especially
protein, is supposed to irritate the tissues so as to stimulate sugar
formation. Therefore the author reiterates Bouchardat's advice,
"manger le moins possible," and particularly restricts protein. He
regards fat as the food which sets up the least stimulus to sugar for-
mation and which never gives rise to glycosuria ( (1), p. 248). He
enforces vegetarianism, because patients are thus kept in equilibrium
on 20 to 25 calories per kilogram of weight with a diet bulky enough to
satisfy, and because he believes that this maintenance requirement is
lower than on animal food, that vegetable protein has a superiority
over animal protein in contradiction to the caloric theory, and that the
vegetable diet is intrinsically less irritating to the diabetic process.
Milk is regarded as somewhat similar. Fast-days are supposed to
benefit through absence of food irritation, but they are held ( (1), p.
252, and elsewhere) to have little practical value, because their effect
is transitory and glycosuria always returns. Kolisch (2) makes a
trenchant criticism of the Kulz method of testing tolerance, objecting
that this shows merely the result of adding relatively small quantities
of carbohydrate to large quantities of protein and fat. Instead, he
advocates trying various combinations of foods, and choosing the one
which permits maintenance on the lowest number of calories, also the
taking of as much carbohydrate as possible without harm. Here a
critic will necessarily ask for a definition of the phrase "without harm."
Von Noorden ( (1), pp. 369, 372) calls attention to the phenomenon
studied by Leo, Rosenfeld, and Kolisch, that up to a certain point
many diabetics assimilate more carbohydrate as the quantity ingested
is increased (paradoxical law) ; the practice of giving such a ration as
will cause the greatest possible combustion of carbohydrate is called
the method of Rosenfeld and Kolisch; von Noorden opposes this
method for mild or moderate cases, but endorses it for severe cases.
Roubitschek and Gaupp are among the recent advocates of this "best

HISTORY 47

oxidation level" program, naming Klotz also in support of it. This is
one phase of the method of the so called "carbohydrate balance," under
which physicians everjrwhere have been greatly concerned over the
relation between the quantity of carbohydrate ingested and the quan-
tity of sugar excreted, and, especially in threatening acidosis, have
juggled the diet in every possible way to make the former greater than
the latter. The method has also been used very widely and by the
highest authorities for the sake of mere comfort and temporary well-
being of the patients; for example, von Noorden's advice, criticized
above by Lenne; the advice of Naunyn ( (4), p. 20) that not more
than 0.5 per cent glycosuria is allowable in mild cases; and the state-
ment of Magnus-Levy ( (2), p. 67) that the advantage of 100 gm.
bread in the diet is worth the excretion of 20 or 25 gm. sugar as long as
no complications are present. This entire method is fundamentally
vicious and in the end defeats every purpose for which it is employed.
On the other hand, there is interest in the view of Kolisch, similar to
that of Lenne, that the patients with milder diabetes are injured by
heavy protein-fat diet, even though glycosuria and other s3anptoms
are absent; and that the ultimate consequence is that they progress
downward and later show the severe form. For such cases Kolisch
.favors a low calory mixed diet, containing little meat and plenty of
vegetables, with carbohydrate in quantity just short of producing
glycosuria.

Albu is the author of the most recent vegetarian system for
diabetics.

Carl Hanko von Noorden has occupied a position of eminence among
diabetic specialists in the generation after Naunyn. He was trained
under Hensen, Riegel, and Gerhardt, has directed important clinics at
Frankfort and Vienna, and by his writings has done much to diffuse
knowledge of the rational treatment of diabetes. The investigations
of his large and influential school are voluminous, but belong
mostly to the theoretical side of the subject. He long maintained the
deficient utilization of carbohydrate in diabetes, but in the later edi-
tions of his text-book went over to the pure overproduction h)rpothesis.
He also supported the polyglandular doctrine, which assails the unity
of diabetes; but, though still nominally defending it, and assigning
great importance to the liver and the thyroid, his later writings con-

48 CHAPTER I

cede the essential contentions of his opponents ((2), p. 69): "But
really these differentiations do not shake the essential unity of the
metabolic disturbance in diabetes in the very least. I think I shall
be voicing the opinion of all pathologists when I say that every indi-
vidual who has a diminished tolerance for carbohydrate, either per-
manently, or extending at least over a considerable period) and thus-
exhibits the most important clinical symptom of diabetes, must be
considered as a subject of pancreatic insufficiency. We need not
always expect to find perceptible anatomical evidence, for there may be
functional impairment where no macroscopic or microscopic patho-
logical appearances can be discovered." Von Noorden has been un-
fortunate in his support of false theories, but he deserves credit as the
principal upholder against the Naunyn school of two doctrines which
now appear to be justified by facts : first, that diabetic acidosis repre-
sents something more than lack of carbohydrate; second, that the
symptoms of acidosis, including the fatal termination, are due to some-
thing more than simple acid intoxication. Von Noorden's clinical
work has consisted chiefly in systematizing and improving the Kiilz;
method in some details. He justifies the Kiilz treatment by the state-
ment that he has under his care some of Kiilz's patients who have re-
mained in good condition for seventeen years. The one distinctive
feature introduced by von Noorden, the oat cure, was previously-
discussed. Though he stands as the most prominent believer in the
formation of sugar from fat, this belief has not influenced his treat-
ment; for he "perhaps gives diabetics greater quantities of fat than-
anybody else;" he regards fat as the anchor of their salvation; he has.
almost never seen increase of glycosuria from it, except when digestive
upsets occur, in which many diabetics immediately excrete more
sugar ( (1), p. 96). Nevertheless he recognizes occasional "fat-sen-
sitive" cases. High fat intake, greatly in excess of the requirement,
is said to increase metabolism, like every overabxmdant diet, and'
therewith increases the sugar excretion. But in order to produce this^
increase of glycosuria, the quantities of fat required are so high as to-
be superfluous and of no practical importance in treatment. In the
presence of severe acidosis, it is held that butter should be avoided,
but that ordinary animal and vegetable fats cause no increase of
ketonuria in a patient accustomed to strict diet ( (1), p. 141), and even*

HISTORY 49

during the transition to strict diet the administration of alkali is an
adequate precaution (p. 293), so that fats are given freely even under
these circumstances. In addition to alkali, von Noorden formerly-
treated impending coma with carbohydrates, especially oatmeal, milk,
and levulose; but recently he has found that one or two fast-days are .
far more effective. On these days the only food is alcohol in large
doses, up to 200 to 250 cc. cognac. As soon as the glycosuria and aci- .
dosis are thus partially controlled, he hastens to inflict an oat cure
( (1), p. 388). Here also the fat intake is limited, thus contradicting
his previous contention. A large proportion of severe cases are con-
ceded to be hopeless ; here a liberal varied diet is allowed, the glyco-
suria being merely limited and the strength maintained ( (1), p. 371;
(2), p. 151) and 15 to 20 gm. sodium bicarbonate and about 6 gm.
calcium carbonate given daily for the acidosis ( (l), p. 389) . Not only
strict diet or vegetable days, but also actual fast-days, are interposed
in this program. ( (2), p. 93) : "There are but few diabetics who do not-
become sugar-free on these days,^' and you will at the same time notice
an enormous fall in the acetonuria. Fast-days, combined with bed
rest, are excellently borne. I never find that the patient's strength
is unduly diminished by them. An important result is regu-
larly attained in the immediate and well-marked rise of tolerance
which follows." Again ( (2), p. 152) : "We need have no fears that the :
hunger day will damage seriously the general nutrition. Of course the
body weight falls on the fast-day, but the loss is rapidly made up, and
by this combined method we often obtain considerable increases in
weight." Von Noorden refers to these fast-days as "metabolic Sun-
days." The metaphor is striking and accurate, but the insufficiency
of the metabolic rest and the attempt to build up weight in the pres-
ence of glycosuria and acidosis are fatal to the patients and to the
method.

Weichselbaum and Stangl in 1901 first observed the specific "hy-
dropic" degeneration of the islands of Langerhans. It is remarkable
that one of the most important contributions to the morphologic

" Remarks of this sort show the actual mildness of many cases classified by
writers as severe.

50 CHAPTER I

pathology of diabetes should have met with such a complete lack of
confirmation or credence.

Among English writers, Williamson in 1898 published a text-Hook
possessing permanent value by reason of the author's great experience
and wide knowledge. Recently (2) he has made some use of a diet
consisting only of casein and cream given in small quantities every
two hours. He attributes the benefit to this latter device and to the
reduction in the total quantity of food, but says: "In the most severe
forms of diabetes with marked diacetic reaction in the urine, I do not
at present feel justified in recommending the casein treatment."

Cammidge ( (1), p. 297) held that with impaired fat metabolism in-
dicated by wasting, lipemia, and acetonuria, a limitation of fat in the
diet and its partial replacement by carbohydrate is advisable, even
though glycosuria be increased. More recently (2) he has advocated
a treatment resembling that of Lenne. He aptly remarks that fat
and protein metaboHsm should be considered as well as that of sugar,
and that the absence of any striking color reaction for protein disturb-
ance, comparable to those for detecting sugar or diacetic acid, goes far
to account for the neglect concerning the protein metabolism. The
treatment consists in reduction of protein, rest in bed, and opium when
nitrogenous equilibrium cannot be established by any other means.
In adopting recently the fasting treatment, he has emphasized the
study of the protein metabolism for judging the condition and progress.

Modern France has not lived up to Bernard and Bouchardat in this
field. Not only has it remained relatively barren of important origi-
nal contributions, but also, outside the practice of a few specialists,
the knowledge and management of diabetes seem to fall below the high
general standard of French medicine. A French physician on a
recent visit to America remarked that patients in France were less
willing than those in other countries to adhere to restricted diet, and
demanded a cure which would enable them to eat freely.

Lepine has published a very large number of studies especially
concerning blood sugar and glycolysis, but his comprehensive text-
book alters nothing in the accepted treatment of diabetes. The
same is true of his recent review of the therapy (2, 3).

Fasting has been employed in diabetes not only by specialists in

HISTORY 51

this subject, but also by enthusiasts who advocate it as a panacea.*'
Of these the most prominent is Guelpa of Paris. Starting from
an incorrect observation of Dujardin-Beaumetz in typhoid fever,
"that the more regular and rapid the patient's loss of weight, up
to the disappearance of the pyrexia, the quicker and more favor-
able was his course to recovery," Guelpa applied the principle first
to infections. "I have found it an invariable rule that, in febrile
affections, the more promptly emaciation sets in, and the more defi-
nitely it establishes itself, the more sure and rapid is the patient's
progress toward recovery. Conversely, when the patient fails to
exhibit an emaciation proportional to the intensity of his pyrexia, the
illness is always graver and of longer duration, and the convalescence
more prolonged and more interrupted. All this, it seemed to me,
proved, so to speak, mathematically, that disease is a state determined
and kept up by the presence within the body of a quantity of products
of fermentations-toxins and the debris of poisoned tissues — which the
organism must eliminate before it can return to a condition of health."
Having set up the theory of autointoxication as the dominant feature
in all disease, Guelpa proposed fasting — ^generally in three-day periods
— as the sovereign remedy. Symptoms of weakness, headache, and
malaise during fasting, and the sensation of hunger itself, were at-
tributed to autointoxication; food relieves the symptoms by com-
bining with the toxin, while purgation also relieves by sweeping out
the toxin; copious purgation — a bottle of hot Hunyadi-Jdnos water
daily — was accordingly added to the treatment. Among the condi-
tions for which the fasting-purgation treatment is recommended, with
confirmatory histories of grateful patients, are gout and rheumatic
troubles, anemia, bronchitis and asthma, herpes zoster, eczema and
other dermatoses, various ophthalmic conditions, some gynecological
conditions (including postpartum hemorrhage), digestive complaints,
nervous disorders, insanity, epilepsy, drug addictions, various infec-

'"' Some of these are outside the ranks of the medical profession. Hereward
Carrington, in his book, "VitaKty, Fasting and Nutrition," New York, 1908, p.
187, mentions a patient with incipient diabetes who fasted twenty days continu-
ously, becoming free from glycosuria and remaining so for two months thereafter,
when he was lost from observation. In the same place is a reference to a previous
example recorded by C. C. Haskell.

52 CHAPTER I

tions, postoperative complications, etc. Important in the list is dia-
betes, where alone the results have attracted widespread notice. A
diabetic is given the usual fasting and purgation for three to five days.
Other features of the treatment are best shown in Guelpa's own words
((5), p. 131):

"It is necessary to insist on the absolute necessity of repeating the cure from time
to time, and of imposing, during the intervals, which should be carefully lengthened,
a carefully restricted diet. As regards the latter, it is my custom to complete the
first period of the cure (three or four days) by a week of mUk diet, the amount of
milk taken daily not to exceed 2J pints. At the end of this week, however satis-
factory the condition of the patient, I prescribe a second period of cure (three or
four days) to be followed by a week or a fortnight of a regime mainly of vege-
tables, which satisfies the patient by fiUing his stomach, but, in reality, under-feeds
him, the object being to continue the process of forcing the organism to live par-
tially on its reserves and to bum off its debris. The following is a menu of the
diet I generally adopt: Breakfast, coffee or tea without milk; Lunch, clear soup,
salad, one or two apples or pears; Dinner, as lunch. As drink, tea or other non-
nutritive drinks ad lib. In certain special conditions I allow an ounce or so of
bread, or a diet of cooked vegetables. I increase the amount of food after each
repetition of the cure, taking as my guide an analysis of the urine. Since I adop-
ted this regime, I have obtained more rapid and stable cures, without discouraging
relapses. I wish also to draw attention to what I believe to be a deplorable error;
namely, the doctrine that milk is very harmful in the treatment of diabetes. This
is a mistaken view, based on a false interpretation of a single fact. It is quite true
that diabetics kept on milk diet almost always pass an increased quantity of sugar.
This increased excretion, is, however, only temporary. From the fact of the in-
creased glycosuria, the conclusion has been drawn that milk is harmful in diabetes.
The deduction is the result of a too superficial process of reasoning. It would be
as logical to conclude that rest and warmth were harmful in the treatment of rheu-
matic conditions, from the fact that they lead to an increased discharge of urates.
In the case we are considering, the milk merely hastens the expulsion of sugar,
which is injuring and impeding the tissues, relieves the hematopoietic fimction,
and contributes to a cure, if the mistake is not made of overwhelming the blood-
forming organs by administering a quantity of milk beyond the metabolic powers
of the liver to deal with."

Afterward, potatoes, bread, and other elements of a mixed ration
are gradually added, with general admonitions against overeating.
Acidosis is not mentioned in the records of Guelpa's early "cures."
About 1911, something seems to have called his attention to acidosis,
for he suddenly (7) added a new chapter to his theory of diabetes.

HISTORY 53

Here he announces that diabetes is the type disease of hyperacidity.
Glycosuria is merely one of the multiple forms of defense of the organ-
ism against acidosis caused by food pernicious in its quantity and es-
pecially in its quality. There are several stages of the process, first
increase of urea, later glycosuria, later acetonuria, etc., and the sixth
and final stage is coma. The body defends itself by breaking down its
less useful elements, notably fat; an indication is the acetonujria, which
like the glycosuria is helpful and not harmful in the process of acidosis.
He denounces the overfeeding in the usual treatment of diabetes, and
denies that his method is unsuited for diabite maigre. As evidence,
he cites the example of a patient aged sixty-five years. This man
underwent a "cure" of five days' fasting with 40 gm. sodium sulfate
daily. The subsequent diet of vegetables, fruits, and 60 gm. bread
daily caused return of glycosuria, whereupon the five-day "cure" was
repeated, followed by a similar diet. The duration of this "dis-
toxication cure" was a month, and the result was that the patient be-
came free from his former glycosuria, albuminuria, and joint infection.
For threatened coma, Guelpa (7 and 11) advises copious drinks and
enemas of sugar and weak alkaline solutions, oxygen inhalations,
bleeding, and intravenous injections of physiological saHne or weak
alkali.

The Guelpa treatment has gained followers chiefly in France
and England. Cammidge ( (1), p. 343) mentions authors reporting
favorable results, but states that he has never been able to persuade
any patient to undergo it. A recent favorable report is by Hume.

Clear recognition should be accorded to Guelpa for the following
points of merit. First: without being guided by knowledge of earlier
undernutrition cures, and entirely from his own original and independ-
ent thought, he devised the first plan of treating diabetes by a radical
initial fast, longer than any previously recommended for this purpose.
Second: these fasts were repeated a number of times, with intervening
periods of diet very low in calories and protein and relatively rich in
carbohydrate, and the increase toward a living ration was made
gradually. Third : he emphasized loss of weight as a potent factor in
the improvement, and carried the reduction of weight to a more ex-
treme point than ventured by anyone before him, and did this even
in patients complaining of weakness. Fourth : he was first to demon-
strate the beneficial effect of fasting upon certain compUcations,

54 CHAPTER I

notably diabetic gangrene. The dietotherapy of gangrene is familiar
in text-books, but the important observation of Guelpa was that fasting
benefited the gangrene, instead of making it worse by weakening the
patient. Fifth: fasting periods were employed not only whenever
glycosuria or other symptoms appeared but also as a prophylactic
against their return. Certain' contrary facts must also be given
proper weight. The Guelpa treatment, in spite of its ease and sim-
plicity, failed of acceptance at the hands of diabetic specialists and
the immense majority of medical practitioners in all countries. The
explanation of this fact necessarily casts discredit either upon the
medical profession or upon this mode of treatment, and the latter
alternative is the true one. It is frequently repeated that the cases
treated successfully by Guelpa's method were severe, and that "the
usual anti-diabetic regime had failed;" but the details of the unsuc-
cessful diets are not given and the assertion cannot be accepted as cor-
rect in a single instance. In age, the patients were almost without ex-
ception above forty and frequently above sixty; many were obese;
their complaints were largely the natural consequence of their mode of
life at their time of life; on cessation of overeating and a lively purge
they were astonished how much better they felt, and their diabetes
was so slight that it was controlled by these simple measures with
little or no subsequent restriction of carbohydrate. The two most
severe cases of the series, namely that of the man described by Arnold*'
and that of the woman described by Bardet,^ cannot be considered

*^ Introduction to translation of Guelpa's book.

*^ Bardet narrates that in the therapeutic clinic of Beaujon was a woman with
diabetes of several years' duration, excreting 800 gm. sugar daily. Emaciation
was not extreme and acutely threatening symptoms were absent. Nothing re-
sembling the Naunyn treatment was undertaken. "She was placed for several
weeks under the ordmary treatment of M. Albert Robin, namely alternate medi-
cation with antipyrine and arsenic, without its being possible to reduce the
quantity of sugar below 160 gm. After a series of this medication, the patient was
left free from all treatment, and followed the routine diet of the diabetics of the
service : meat 500 gm., potatoes 500 gm., green vegetables 500 gm. At the time of
beginnmg the experiment (i.e. absolute fasting), she was passing 12 liters of urine in
24 hours, and on the final day showed an eh'mination of 760 gm. sugar." Here is
seen a combmation still too frequent in all countries; absence of rational treat-
ment, dependence on drugs, the use of routine instead of individualized diets, and
the physician's ignorance that the alleged sugar excretion on the diet stated is
impossible.

HISTORY 55

examples of severe diabetes; at the utmost, they would fall in the class
of "medium severity" according to von Noorden or Naunyn; they are
of the type easily cleared up under the Naunyn plan of regulated diet,
restricted protein, and intercalated fast-days, and neither of them
remained clear Tender the Guelpa method. So far from this method
being an improvement over the known treatment, a physician con-
fronted with the choice of referring a patient to Guelpa or to Naunyn
could have no possible ground for hesitation in choosing the latter.
The Guelpa plan is applicable only to mild diabetes, and here (not-
withstanding the quick temporary clearing of glycosuria) a permanent
success is attained only in a longer, harder, and less certain manner
than under the usual treatment. For diabetes of even moderate
severity, the attempt to fast, purge, and undernourish a patient until
he is able to tolerate carbohydrate-rich diet is inevitably disastrous.
In undertaking to apply the mode of treatment described in the pres-
ent monograph, the most common difl&culty and mistake of inexperi-
enced physicians has been to fast the patient till free from glycosuria,
then to give a diet permitting its return, then to fast, then to proceed
with improper diet, so that weight and strength are lost while tolerance
is injured instead of improved, and the end in any severe case will be
fatal. In the one young patient of his series, a youth of sixteen years,
with actually severe diabetes, Guelpa ( (5), p. 112) achieved sugar-
freedom after fifteen days, but relapse followed because the patient
finally found the program unendurable. There may be justifiable
surprise that Guelpa describes only successes; in his half dozen or less
of partially successful cases the blame for mishaps is placed entirely
upon the patients. Inasmuch as common knowledge and Guelpa's own
experience ( (1), p. 506) make it clear that purgation does not prevent
acidosis during fasting, it would be remarkable if so many diabetics
should be treated without encountering some of those severe cases of
long standing who go into fatal acidosis on fasting. There is still more
noteworthy absence of a record of any young patient with impending
coma who was cleared up and kept clear of both glycosuria and aci-
dosis. It is improbable that Guelpa avoided such cases altogether;
it is certain that his treatment must fail in the vast majority of them;
and his record of success limited to mild cases constitutes sufficient
evidence of his failure in more severe cases, even of the grade that can

56 CHAPTER I

be managed successfully under the Naunyn plan. On the one hand,
Guelpa should receive due credit for boldness, enthusia,sm, originality,
and some new observations growing out of a new clinical procedure.
On the other hand, it cannot be maintained that Guelpa devised a
good treatment for diabetes. The lesson of his work cannot be over-
looked; but the information and encouragement derivable from his

'long fasts in mild cases are less than from the shorter fasts of Naunyn
and von Noorden in severe cases, so that the proposed treatment of
severe cases by fasting is a development of the Naunyn method rather
than of the Guelpa method.

America has not been prolific of diabetic text-books. A notable
early example is that of Tyson, the frontispiece of which shows the
intraocular picture by which diabetic lipemia can be diagnosed.
■ The &st great contribution of this country to this subject was
Opie's hypothesis that diabetes is due to alterations in the islands of
Langerhans, on the basis of findings of hyaline, fibrous, and other
destructive changes in the islands in a series of cases where the acinar

■ tissue was relatively little affected.

Mandel and Lusk demonstrated the dextrose-nitrogen ratio of the
phloridzinized dog in a human diabetic, and drew attention to the
prognostic value of this ratio. Lusk's "Science of Nutrition" treats
a subject of such dominant importance for intelligent dietotherapy
that it may be placed in the highest rank among text-books of diabetes.
The most extensive investigation of the respiratory metabolism in
diabetes is that of Benedict and Joslin.

Hodgson treated over 1100 patients in the twenty years preceding
1911. He worked out a plan of treatment without drugs, using a
mildly alkaline mineral water freely. He held that patients "should be

kept mentally indolent and physically active One other

essential must be made' plain to the diabetic, and that is the quantity of

food eaten is just as important as the kind of food It is a

fact that many mild cases of diabetes will show a diminution of sugar
almost to the vanishing point when the patient is merely compelled
to eat a very moderate ordinary diet. That is to say an antidiabetic
diet is not always necessary to reduce the glycosuria; a reduction in the
amount of ordinary food will sometimes accomplish the same end.

' . . . . Again it should be stated that the quantity of all food, even

HISTORY 57

if it is carbohydrate-free, must be greatly restricted. The number of
calories that the body ordinarily requires is no safe criterion for the
amount of food that should be given a diabetic. It is not the quantity
of food that should be metabolized, but the quantity that can be me-
taboUzed that should determine the amount given to the patient. All
in excess of the quantity that the patient can actually use burdens the
already overtaxed excretory organs and retards improvement." In cases
severe enough that sugar did not disappear after two weeks of strict
diet, the patient was put to bed and allowed one raw egg and two
ounces of olive oil three or four times a day. If diacetic acid appeared,
the oil was diminished and some carbohydrate added. Hodgson's
statistics show a high percentage of favorable results in cases not too
severe in t}T)e.

Foster's manual (1915) is not only an excellent brief presentation of
the Naunyn system, but distinctly goes beyond this in the more radical
employment of undernutrition, with correspondingly better results.
He lays down the wise rule (p. 165) in contradiction to some European
authorities, that it is not safe to disregard diabetes even in advanced
life. By the use of repeated fast-days, vegetable days, and restricted
diet he achieves freedom from glycosuria in cases of the type given up
as hopeless by many writers. The procedure in such cases is slow,
and the control transitory (p. 216). "By the enforcement of rest in
bed and a stringent diet the urine can be freed of sugar in the vast
majority of cases. With early cases the result is often effected within
a few days; when the disease is advanced and there is a complicating

severe acidosis, months may be necessary These are the

most discouraging cases, as they never approach a semblance of health.
. . . . At once on beiiig released from incessant control, there is
an inevitable transgression beyond the path of safety in diet and exer-
cise. . . . . With severe cases of diabetes coma develops finally
in spite of the best endeavors."

Mosenthal applied the hospital class system to the care of diabetics.**
The method is particularly adapted to a disease in which instruction
of patients is so essential as in diabetes, and it is the most effective
practical measure in the organization of a clinic, both for the care of

^' Cf . Joslin ( (4), pp. 327 and 409) .

58 CHAPTER I

ambulant cases and for guarding against relapse in patients after dis-
charge from hospital. More widespread and effective social service
along these lines offers one of the most important means of diminishing
the death rate from diabetes.

Woodyatt (1) was one of the very few who in 1909 held clearly to
the conception of diabetes as a deficiency of the internal function of the
pancreas.'** Woodyatt (3) has recently suggested that the weakness
of the pancreatic function here concerned may not always be an in-
herited or constitutional defect in the Naunyn sense, but may some-
times be acquired, especially through infections which selectively
injure either the pancreas or the nervous mechanism cohtroUing it.

^ "Diabetes mellitus is a disease in which the body has in part lost its ability
to utilize sugars. Sugar arrives at the point where it should burn, but fails to do
so, and accumulating in the blood creates an hyperglycemia. Disregarding acces-
sory factors, which may play a part, we can say that ultimately the failure of sugar
combustion in diabetes mellitus depends upon lack of 'a something derived from
the pancreas.' The pancreas, like other glands, is capable of being stimulated intO'
a state of fatigue. It may be conceived that excess of sugar in the blood of healthy
individuals acts directly or indirectly (e.g. through nerves) as a stimulus to the
pancreas, as a result of which more internal secretion is set free and the excess of
sugar thereby automatically taken care of. This removed, the stimulating in-
fluence ceases and the pancreas rests. In diabetes it may be assumed that the
pancreas is functionally weak. A small excess of sugar in the blood, let us say,.
calls for a response from the pancreas, and as in health the excess may be removed.
Sooner or later, perhaps as a result of some dietary excess, or of some shock to the
nervous system which results in an outgush of sugar from the glycogen depots of
the liver, an unusual hyperglycemia occurs. This calls for a strong pancreatic
response, more than the functionally weak gland can give, and some excess of
sugar remains unutihzed in the blood. If hyperglycemia persists for any appreci-
able time the continuous pancreatic stimulation thereby engendered results in
glandular fatigue. Less and less secretion is elaborated, less and less sugar utilized,
the hyperglycemia grows progressively worse and a vicious circle becomes es-
tablished. The condition of the pancreas then corresponds to that of a heart with
broken compensation, and as the treatment for such a cardiac condition is rest, so
in diabetes rest is needed for the pancreas. To secure this we must control the
stimulating hyperglycemia, which means primarily the withdrawal of carbohy-
drates from the diet, secondarily reduction in the amount of protein, until absence
of glycosuria tells us that the blood sugar percentage is approximately normal.
After prolonged rest of this sort a return of the pancreatic function to its previous-
state is frequently spoken of as an increased body 'tolerance for sugar.'

Such restoration of sugar-burning capacity, such increase in 'tolerance' is the-

HISTORY 59

Raulston and Woodyatt in 1914 described a case of diabetes, for which
fasting had been used.^* Woodyatt (2) said at a symposium on dia-
betes before the Association of American Physicians in 1915: "For
eight years at the Presbyterian Hospital we have regularly used starva-
tion in the treatment of diabetes, following principles with which I
became acquainted in the clinic of Muller in Munich. We have fasted
patients for the purpose of desugarization for periods of one, two,
three, and in one case five days, and have kept patients for prolonged
' periods in semistarvation. There can be no doubt of its value in cer-
tain phases of treatment. As to its safety, I have seen two deaths
apparently from spread of infection immediately following a period
of fasting."

first aim of diabetic therapy. There are cases in which the ability of the
body to utilize carbohydrate has sunk so low that as a result certain secondary
changes in the fat metabolism have supervened. These changes are mainly re-
sponsible for the condition spoken of as acidosis. In health and in diabetes with-
drawal of carbohydrate from the diet frequently causes the appearance of a pre-
viously absent acidosis or an increase in the severity of an already existing one.
These aggravations are temporary. Still in such cases as already have a danger-
ously large amount of the acetone bodies in the blood no increase at all is per-
missible. In these cases, and only in these cases, should one refrain from an at-
tempt to improve tolerance. Just where to draw the line is a matter for individ-
ual judgment. Where means are at hand for accurate quantitative measurements
of the daily excretion of acetone bodies one may be justified in closely approaching
the danger point. When these means are not available a more respectful margin
of safety must be maintained."

*^ "We made a transfusion of blood into the veins of a patient suflfering from
diabetes mellitus, one for whom all known expedients had been exhausted and who

was approaching the end The patient, a man, aged thirty-four, had

first shownsymptomsofdiabetessixyearspreviously For two years the

symptoms had been severe, and for eighteen months prior to the transfusion he
had been constantly under observation in the Presbyterian Hospital, Chicago,
where on numerous occasions his metabolism had been studied for prolonged
periods. Prior to entering he had twice become unconscious with what had been
diagnosed as diabetic coma, and on several occasions afterward coma was
averted only by the enforcement of complete bodily rest and the use of maximum
doses of alkali and wine. He became fully educated with regard to the require-
ments of a metabolism study and voluntarily cooperated in a highly intelligent
way. He knew that the expectancy of life was very limited and solicited the
trying of any new line that might even temporarily mitigate his condition or

60 CHAPTER I

In the same discussion, Billings (1) spoke to similar effect.*^ Re-
cently Billings (2) has written, "In the service of the Editor in the
Presbyterian Hospital, Chicago, in collaboration with Dr. R. T.
Woodyatt, the treatment of diabetes by a preliminary absolute fasting
period, until the urine is sugar-free, has been followed for nine years.
We have fasted patients for as long as eight days. The patient is
encouraged to drink water freely. Acidosis usually diminishes
rapidly. One may give whisky or sour wine during the fasting period.
Soda bicarbonate may also be used in persistent acidosis. All that is '
said by Allen and Joslin concerning the treatment we can afSrm."

I^o clear up possible misunderstandings, the following may be
remarked:

(1) Friedrich Miiller has published nothing in regard to the principles attributed
to him. On the contrary, Staubli published (1908) the records of one clinic patient
and two private patients of Friedrich Miiller, showing that they were treated by
the Naunyn method, and though the treatment continued for a number
of months and the cases were not extremely severe, they continually showed marked
glycosuria and ketonuria and were dismissed with these still present. Further-
delay the end. On several occasions his glucose to nitrogen ratio closely approx-
imated 3.65 : 1 on a diet aggregating 2,500 calories (due allowance having been
made for ingested carbohydrate). Nevertheless his urine coiild always be
rendered sugar-free by fasting, and on semistaryation (the Falta-Lusk quotient)
could be reduced from 100 or thereabouts to the neighborhood of 50, as it was on
the diet used at the time of transfusion. During the time of observation the
patient remaiaed quietly in bed. Diet. — For two weeks prior to the transfusion
and for five days afterward the diet consisted of 800 cc. of 16 per cent cream, three
eggs (150 gm.), and water, clear tea or coffee to make the total volume of fluid two
liters daily." The patient died shortly after this time.

** "I am surprised to hear it said that the method of starvation of diabeticpatients
is new. We have used that method in Chicago for a number of years and patients
have been fasted for as long as eight days. The adoption of the method there was
due to the work of Woodyatt. A point to be remembered is that the study of
patients at rest in a hospital is only part of the problem; it is necessary to study
them after exercise, after return to ordinary mode of life. For years, I have taught
patients how to examine their own urine. While it may be harmful to give fats in
general in diabetes, butter fat is not harmful. Diabetics may take butter fat or
bacon fat and may do so for years. Whatever may be said, it is impossible ever
really to control diabetic patients; they will do as they please as soon as they get
beyond the observation of the doctor."

HISTORY 61

more, personal letters recently received show that Friedrich Miiller has no knowl-
edge of the proposed treatment, and considers it theoretically inadvisable because
of the supposed danger of acidosis.*' Such an attitude on the part of one so
widely informed concerning diabetes and so familiar with the Naunyn method,
affords some evidence of the newness of the proposed treatment and the principles
underlying it.

(2) Though Woodyatt states (1915) that an initial fast has been used for eight
years, and Billings (1916) that it has been used for nine years, the above quoted
therapeutic program of Woodyatt (1) makes no mention of the use of such a
method in 1909; on the contrary, it is there advised, in harmony with Naunyn,
that in cases with very dangerous acidosis one should "refrain from an attempt to
improve tolerance." No description of the new method has since been pubHshed
by either of these authors.

(3) The paper of Raulston and Woodyatt makes incidental reference to fasting
and semistarvation. It seems evident that the plan of fasting used and referred to
by these authors resembled that of von Noorden, the only difference being that the
periods were sometimes longer; the effect is a temporary cessation of glycosuria

*' One letter was addressed to Professor Graham Lusk, and another to one of the
present authors. Liberty is taken to quote from the latter, under date of August
1,1915.

"Die Frage einer kalorisch armen Ernahrung bei Diabetes ist vor einigen Jahren
in der deutschen Literatur durch Schlesinger erortert worden, und er hat gezeigt,
dass Diabetiker haufig bei einer an kalorieri auffallend armen Nahrung sich erhal-
ten. Ein Nutzen fiir die Kranken wird aus dieser Arbeit nicht erkenntlich. Dann
hat Weintraud vor Jahren in seinen aus der Naunynschen Klinik kommenden in
der Bibliotheka medica erschienenen Arbeit auf die Bedeutung einer zeitweiligen
Unteremahrung hingewiesen, und Sie finden diese Gesichtspunkte in dem Buch von
Naunyn iiber Diabetes ausfiihrlich dargelegt. Wir verwenden in Deutschland
zeitweiUge Unteremahrung, sogenannte Hungertage, ganz gewohnHch zur Re-
duktion des Zuckers, und scheuen uns nicht das Korpergewicht dadiirch zu re-
duzieren. Freilich gelingt es nur selten durch solche Hungertage die Acidosis zu
vermindern, da ja der Hunger an sich auch bei gesunden Menschen ausgesprochene
Acidosis zu erzeugen pflegt. Jeder Hungerzustand fiihrt zu Verbrennung von
Korperfett imd erzeugt daher bei Mangel an Glykogen eine Acidosis. Bei Dia-
betes, wo der Glykogenvorrat ohnedies reduziert ist, und wo die Zuckerverbren-
nung haufig schwer geschadigt ist, tritt die Hungeracidosis gewohnlich noch
starker hervor, und erschwert die Behandlung durch Unteremahrung. Eine
generelle Verordnung der Unterernahrang bei Diabetes dtirfte schon aus dem
Grunde nicht ganz ohne Bedenken sein, well die Diabetiker unter einander so un-
geheuere Verschiedenheiten zeigen, dass man sich hiiten muss alle Falle nach der-
selben Regel zu behandeln. Das letzte Wort in dieser Frage hat jedenfalls nur die
Erfahrung, nicht aber die Theorie."

62 CHAPTER I

and diminution of ketonuria at the price of a certain amount of weiglit and nutri-
tion, but the diet after the fast permits a quick return of the symptoms. It is
expressly stated that in the semistarvation periods the Falta-Lusk quotient^* was
still about 50, which means serious glycosuria; and it is obvious that marked
ketonuria was constantly present. Billings' opinion concerning fat, and the high
fat diet used by Raulston and Woodyatt, suffice to explain such a result, for without
fat restriction these patients cannot be kept free from such symptoms.

Misunderstanding of the incomplete description of the method in the brief pre-
liminary communications was evidently responsible for the early criticisms of this
character. Aside from the fundamentally new principle of total caloric regulation,
it has been necessary to develop many practical details. The discussion of the
resulting system has in general remained free from questions of priority.

Joslin has had the largest experience in the treatment of severe dia-
betes in this country, and has published the latest as well as the most
advanced and authoritative text-book. No other American clinician
has followed the scientific study of diabetes so long and intensely.
His careful records cover approximately 1000 diabetic patients treated
during the past eighteen years, and are particularly valuable because
the great majority of the cases have been accurately followed up to
death or to the present time. His definition is one which when gener-
ally adopted will tend to lower the death rate from diabetes and its
complications. "My rule in the treatment of diabetes is to consider
any patient to have diabetes mellitus and treat him as such, until the
contrary is proven, who has sugar in the urine demonstrable by any of
the common tests. This method of procedure is safer for the patient
than to make use of the term glycosuria, which begets indifference."
He has laid emphasis upon the necessity of keeping patients supplied
with sufficient quantities of fluid and salts. He has been closely in
touch with the development of the fasting treatment from the outset.
He was informed in advance concerning the first clinical results, and
has treated a greater number of severe cases of diabetes by this method
than any other individual. The rapid general adoption of the method
has been largely due to his example and influence, and in his various
publications he has formulated a detailed program which many prac-
titioners have followed. The reversal of conditions is shown by the
fact that whereas fat was formerly the only food not restricted,

«Cf.Lusk(2).

HISTORY 63

Joslin now begins treatment by withdrawing only fat. His statistics
-support the belief that the life of diabetic patients is lengthened by the
new method, and in his judgment they enjoy also better strength and
'Comfort. References to and comparison with Joslin's results afford
valuable information on the questions discussed in the ensuing chap-
ters, and certain topics can be here omitted altogether because of the
manner in which he has handled them on the basis of a wider experience.

One of the present writers*' previously published work which seemed
to promise the possibility of investigating diabetic therapy by animal
experiments. The conception underlying the subsequent research at
this Institute had a threefold origin. One lay in considerations from
the literature as above mentioned, and also the reports of cessation of
'diabetes in various forms of cachexia {loc. cit., p. 800 ff.). The second
was found in certain of the preceding observations; viz., that in dogs
with severe diabetes not too far advanced, glycosuria ceased and tiie
diabetes seemed more or less improved on fasting alone {loc. cit., p. 480,
Dog 64), or together with ligation of the pancreatic duct (Chapter
XXII). The latter experiments were repeated and the role of im-
paired food absorption and undernutrition demonstrated by Homans.
The third suggestion was furnished by Joslin,^" who in a conversation
-called attention to his observations that though infections are gener-
;ally so serious in diabetes, tuberculosis with rapid emaciation had
•seemed sometimes, notably in one very carefully studied case, to be
.accompanied by diminution of both glycosuria and acidosis.

On these various grounds, animal experiments were begun with a
view to the possibility that diabetes is a disorder of the total metabo-
lism and not of carbohydrate utihzation alone, that the entire diet and
maintenance of the entire body mass constitute a load upon the inter-
nal function of the pancreas, and that accordingly in the treatment of
•diabetes increase of diet and of body weight increases the strain upon
this function, and reduction of the total diet and weight relieves this
;;strain more effectively and permanently than restriction of carbo-
hydrate alone. A series of animal experiments seemed to support this

« Allen (1).

^ Cf. Benedict and Joslin, p. 55, Case R; also Joslin, Treatment of Diabetes
:Mellitus, 2nd edition, 1917, p. 409.

64 CHAPTER I

conception, which was then applied to the treatment of diabetic
patients. Some of the results have been outlined in preliminary
communications, which, however, have not been sufficient to convey
an accurate knowledge of the details, and results have varied somewhat
with the different appHcations of the method in different hands.

Among authors who have reported favorable experiences are: in
America, Barker, Bookman, Christian, Friedenwald and Limbaugh,
Greeley, Halsey, Hamburger, Heffron, Heyn and Hawley, Hill and
Eckman, Hill and Sherrick, Jeans, Jones, Lemann, Levy, Lovewell,
Marshall, Martin and Mason, McNabb, Moses, Paley, Potter, Rob-
bins, Stengel and collaborators, Strouse, and Wilhams; in England,
Cammidge, Fenwick, Leyton, Spriggs, and speakers discussing their
papers; in Ireland, Nesbitt; in India, Waters. Its adoption by
speciahsts and institutions, and by a still greater number of general
practitioners, has furnished gratifying evidence not only of its theo-
retical soundness but also of its feasibihty for successful practical
application under the many varied conditions of medical work and
environment. Geyelin and DuBois, and Jonas and Pepper, have
demonstrated the possibility of beneficial results in the most intense
uncomplicated cases ever described in the literature of diabetes.

Aside from any benefits inherent in the treatment itself, it has
apparently served to stimulate interest in diabetes among members of
the medical profession, and to promote the understanding and employ-
ment of rational dietetic management of this disorder, than which
none has been more poorly understood or treated. Such knowledge
and confidence concerning the rational therapy will diminish the use
of the worthless or harmful remedies which appeal to ignorance or
despair. The history of the development of the scientific treatment,
and of some among the many contributors to it, may;fittingly be closed
with a quotation from Naunyn ( (5) , p. 452) . "The interest in novelty
may be granted also to physicians, and the lack of prejudice with
which we accept for trial all things, even the strangest and from the
worst source, may — so far as one may believe in it — ^be praised; but
every physician must beware of undertaking such special treatments
or of recommending them, without ascertaining their relation to what
science has estabHshed and teaches concerning the therapy of our
disease. If this is not possible for him, then the employment of them

HISTORY 65

is not permissible. The therapy of diabetes has been well founded by
painstaking labor highly fruitful in all directions; we may be proud of
that which has been achieved and attained here. The physician who
here frivolously abandons the scientific basis must, if he wishes to be
deemed honorable, submit to the accusation of ignorance."

BIBLIOGRAPHY.

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66 CHAPTER I

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(3) Les hydrates de carbone dans le traitement du diabete sucre, Semaine

mid., 1911, xxxi, 313-318.
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cii, 1240-1242.
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1054.
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Paris, 1851.
(2) De la glycosurie ou diabete sucre, Paris, 1875.
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(2) The Nitrogen Balance in Diabetes MeUitus and Its Importance in

Treatment, Lancet, 1915, ii, 1187-1189.

(3) The New Dietetic Treatment of Diabetes, Ibid., 1917, ii, 522-527.

(4) The New Dietetic Treatment of Diabetes, Brit. Med. J., 1917, i, 503-505.

(5) The Importance of Regulating the Fat-Intake in Diabetes Mellitus,

Ibid., 1918, i, 393-395.
Camplin, J. M., On Diabetes, and Its Successful Treatment, London, 1858.
Cantani, A., (1) Der Diabetes mellitus, translation by Siegfried Hahn, Berlin, 1877.
(2) Le diabete sucre et son traitement dietetique, translation by H. Charvet,
Paris, 1878.
Cawley, T., A singular Case of Diabetes, consisting entirely in the Quality of
the Urine: with an Inquiry into the different Theories of that Dis-
ease, London Med. J., 1788, ix, 286-308.
Chevallier, a., Sur I'urine des diab6tiques, J. chim. mSd., pharm., et toxical.,

1829, V, 7-12. Ref. by Griesinger.
Chevreul, (1) Note sur le sucre de diabetes. Bull. Soc. philomatique, 1815,
148-149.
(2) Note sur le sucre de diabetes, Ann. chim. et phys., 1815, xcix, 319-320
Ref. by Lepine.

HISTORY 67

Christian, H. A., The Starvation Method versus Gradual Carbohydrate Re-
duction as a Time Saver in the Treatment of Diabetes, Boston Med.

and Surg. J., 1915, ckxii, 929-933.
Christie, T., Notes on Diabetes Mellitus, as It Occurs in Ceylon, Edinburgh

Med. and Surg. J., 1811, vii, 285-299.
CsONKA, F. A., The Fate of Ingested Starch in Phlorhizin Diabetes, J. Biol.

Chew.., 1916, xxvi, 327-329.
CuLLEN, G. E., Studies of Acidosis. III. The Electrometric Titration of Plasma

as a Measure of Its Alkaline Reserve, J. Biol. Chem., 1917, xxx,

369-388.
CuLLEN, W., (1) First Lines on the Practice of Physic, Edinburgh, 1st edition,

1776-1784.
(2) Synopsis Nosologiae Methodicae, Edinburgh, 1769. Ref. in texts.
DiNGUizLi, Diabete sucre et son traitement sans regime, d'apres les auteurs

arabes anciens. Bull. Acad, mid., 1913, Ixx, 629-635. (Report by A.

Robin.)
DoBSON, M., Experiments and Observations on the Urine in Diabetes, Medical

Observations and Inquiries by a Society of Physicians in London,

1776, V, 298.
DoNKiN, A. S., (1) On the Relation between Diabetes and Food and Its Appli-
cation to the Treatment of the Disease, London, 1875.
(2) The Skim-Milk Treatment of Diabetes and Bright's Disease, London,

1871.
VON During, A., Ursache und Heilung des Diabetes mellitus, Hanover, 2nd

edition, 1875. Ursache und Heilung der Zuckerkrankheit, Hanover,

5th edition, 1905.
DuPTJYTREN and Thenard, Memoire sur le diabetes sucre, /. med., chir.,

pharm., etc., 1806, xii, 77-111; Bull. Faculte Med. Paris, 1812,

i (1806), 37-42.
Ebstein, W., (1) Uber Driisenepithelnekrosen beim Diabetes mellitus mit be-

sonderer Beriicksichtigung des diabetischen Coma, Deutsch. Arch.

klin. Med., 1881, xxviii, 143-242.

(2) Die Zuckerharnruhr, ihre Theorie and Praxis, Wiesbaden, 1887.

(3) Ueber die Lebensweise der Zuckerkranken, Wiesbaden, 2nd edition,

1898.

(4) Beitrag zum respiratorischen Gaswechsel bei der Zuckerkrankheit,

Deutsch. med. Woch., 1898, xxiv, 101-102.
Falta, W., (1) Die Therapie des Diabetes mellitus, Ergebn. inn. Med. u. Kinderh.,

1908, ii, 74-141.
(2) Ueber die gemischte Amylazeenkur bei Diabetes mellitus, Milnch.

med. Woch., 1914, Ixi, 1218-1220.
Faroes, F., L'assimilation du sucre de lait chez le diabetique; une therapeutique

rationelle du diabete, Gaz. hebd. sc. mid. Bo^(ieoMx, 1915, xxxvi, 33-37.

68 CHAPTER I

Feeling, H., Ueber die quantitative Bestimmung von Zucker und Starkemehl
mittelst Kupfervitriol, Ann. Chem. et Pharm., 1849, Ixxii, 106-113;
Chem. Pharm. Centr., 1850, xxi, 244-246.

Fenwick, p. C. C, Notes on the Starvation Treatment of a Young Diabetic,
Lancet, 1917, i, 299.

FiTZ, R., (1) Acetone Bodies in the Blood in Diabetes, Tr. Assn. Am. Phys.,
1917, xxxix, 155-158.
(2) Observations on Kidney Function in Diabetes Mellitus, Arch. Int.
Med., 1917, xx; 809-827.

FiTZ, R., and Van Slyke, D. D., Studies of Acidosis. IV, The Relationship be-
tween Alkaline Reserve and Acid Excretion, /. Biol. Chem., 1917,
XXX, 389-400. , ■

Foster, N. B., Diabetes Mellitus, Philadelphia and London, 1915.

VON Freeichs, F. T., (1) R. Wagner's Handworterbuch der Physiol., 1846, iii,
'part 1), 803.

(2) Ueber den plotzlichen Tod und fiber das Coma bei Diabetes (dia-

betische Intoxication), Z. klin. Med., 1883, vi, 1-53.

(3) Ueber den Diabetes, Berlin, 1884.

Friedenwald, J., and Limbaugh, L., The Allen Treatment of Diabetes, Inter-
state Med. J., 1916, xxiii, 73-79.

Gerhaedt, C, Zur Aetiologie und Therapie des ninden Magetageschwlirs, Wien.
med. Presse, 1868, vi, 1.

Geyelin, H. R., and Du Bois, E. F., A Case of Diabetes of Maximum Severity
with Marked Improvement. A Study of Blood, Urine and Respira-
tory Metabolism, J. Am. Med. Assn., 1916, Ixvi, 1532.

Greeley, H. P., Diabetes Mellitus. Broader Aspects of Treatment and Re-
sults, J. Am. Med. Assn., 1917, Ixviii, 1685-1689.

Gregory, G., Elements of the Theory and Practice of Physic, London^ 2nd
edition, 1825.

Griesinger, W., Studien iiber Diabetes, Arch, physiol. Heilk., 1859, iii, 1-75.

Guelpa, G., (1) Cure du diabete (and Discussion), Bull. gin. thSrap., 1909,
clvii, 91-105, 494-508; Nouvelle contribution a I'dtude da la purga-
tion. Ibid., 770-789.

(2) Sur la purgation. Ibid., 1909, clviii, 182-189, 213-221.

(3) R6sultats eloignes de 19 cas de diabete trait^s par la m6thode de desin-

toxication, Ibid., 1910, clix, 213-221.

(4) Autointoxication et disintoxication, Paris, 1910.

(5) Autointoxication and Disintoxication, translation by F. S. Arnold, New

York, 1912.

(6) Starvation and Purgation in the Relief of Disease, Brit. Med. J., 1910,

ii, 1050-1051.

(7) Interpr6tation des manifestations diab6tiques, traitement du diabete,

Bull. gSn. thirap., 1911, clxii, 925-931.

(8) La goutte, son traitement, Ibid., 1912, clxiv, 709-716.

HISTORY 69

GuELPA, G., (9) Hygiene des chevaux et regime vegetarian. La goutte, (review
in Lyon Mid., 1913, cxxi, 1082-1084).

(10) Proc. Internal. Cong. Med., 1913, vi, 392, (brief remark).

(11) Desintoxication de I'organisme, Paris, 1913, (review in Lyon MSd.,

1913, cxx, 1204-1206).
GuELPA, G., and Makie, A., La lutte contre I'epilepsie par la disintoxication et

par la reeducation alimentaire. Bull. gin. ihhrap., 1910, clx, 616-624.
Hallervorden, E., Ueber Ausscheidung von Ammoniak im Urin bei patholo-

gischen Zustanden, Arch. exp. Path. u. Pharm., 1880, xii, 237-275.
Halsey, J. T., (1) The Allen Treatment of Diabetes, New Orleans Med. and

Surg. J., 1915-16, Ixviii, 501-509.
(2) The Dietetic Treatment of Surgical Diabetes, South Texas Med. Rec,

1916, X, 10-13.
Hambitrger, W. W., The Allen Treatment of Diabetes, Med. Clinics Chicago,

1916, i, 1051-1075.
Harley, G., Diabetes, Its Various Forms and Different Treatments, London,

1866.
Heffron, J. L., The New Conception of Diabetes and Its Treatment, iV. Y. State

J. Med., 1916, xvi, 69-71.
Heyn, L. G., and Hawley, P. R., The Allen Treatment of Diabetes Mellitus,

Lancet-Clinic, 1915, cxiv, 42-45.
Hill, L. W., and Eckman, R. S., The Starvation Treatment of Diabetes. With

a Series of Graduated Diets, Boston, 1915, 1916, 1917.
Hill, L. W., and Sherrick, J. L., Report on the Allen Treatment of Diabetes,

Boston Med. and Surg. J., 1915, clxxii, 696-700.
HiRSCH, A., Handbook of Geographical and Historical Pathology, translation

by Charles Creighton, New Sydenham Society, London, 1885, ii.
Hirschfeld, F., Ueber eine neue klinische Form des Diabetes, Z. kUn. Med.,

1891, xix, 294-304, 325-359.
Hodgson, A. J., Treatment of Diabetes Mellitus, /. Am. Med. Assn., 1911, Ixvii,

1187-1191. Diabetes Mellitus, Canad. Med. Assn. J., 1912, xli, 874-

891.
Homans, J., A Study of Experimental Diabetes in the Canine and Its Relation

to Human Diabetes, /. Med. Research, 1915-16, xxxiii, 1-51.
Home, F., Clinical Experiments, Histories, and Dissections, Edinburgh, 1780.

Ref. in texts.
Hopkins, F. G., Dr. Pavy and Diabetes, Science Prog., 1912, vii, 13-47.
IwAi, T., Le diabete sucr6 chez les Japonais, et son 6tude comparative avec le

diabete observg en Europe et en Am6rique, Arch. mid. exp. et anat.

path., 1916, xxvii, 1-54, translation by J. LeGoS.
Jastrowitz, H., Experimentelle Untersuchungen iiber die therapeutische Wir-

kungsweise des Hafermehles, Z. exp. Path. u. Therap., 1912-13, xii,

207-220.

70 CHAPTER I

Jonas, L., and Pepper, 0. H. P., Acute Diabetes with Enormous Elimination of

Nitrogen: Report of Case with at Least Temporary Recovery, /. Ant.

Med. Assn., 1917, kviii, 1896-1897.
Jones, N. W., On the Clinical Application of the Newer Methods of Treatment

of Diabetes Mellitus, Northwest Med., 1917, xvi, 38-41.
JosLiN, E. P., (1) Present-Day Treatment and Prognosis in Diabetes, Am. J.

Med. Sc, 1915, cl, 485-496.

(2) Carbohydrate Utilization in Diabetes, Arch. Int. Med., 1915, xvi, 693-

732.

(3) Pregnancy and Diabetes Mellitus, Boston Med. and Surg. J., 1915,

clxxiii, 841-849.

(4) The Treatment of Diabetes Mellitus, Philadelphia and New York, 1916,

2nd edition, 1917.
JosLiN, E. P., Brigham, F. G., and Hoenor, A. A., An Analysis of Fourteen

Cases of Diabetes Mellitus Unsuccessfully Treated by Fasting,

Boston Med. and Surg. J., 1916, clxxiv, 371-378, 425-429.
Kahn, M., and Kahn, M. H., Lime Therapy of Diabetes, Med. Rec, 1915,

Ixxxviii, 744-746.
The Lime Deficiency of Diabetes, Arch. Int. Med., 1916, xviii, 212-227.
Kaeell, P., De la cure de lait, Arch. gin. med., 1866, (2), 513-533, 694-704.
Kaulich, J., Ueber Acetonbildung im thierischen Organismus, Vrtljschr. prakt.

Heilk., 1860, Ixvii, 58-72.
Klemperer, G., (1) Ueber regulatorische Glykosurie und renalen Diabetes (Dis-
cussion), Berl. klin. Woch., 1896, xxxiii, 571.
(2) Die Verwertung reinen Traubenzuckers bei schweren Diabetikern,

Therap. Gegenw., 1911, lii, 447-452.
KoLiscH, R., (1) Lehrbuch der diatetischen Therapie, Leipsic and Vienna,

1899.
(2) Zur d'atetischen Behandlung des Diabetes mellitus, Wien. klin. Woch.,

1899, xii, 1305-1308.
KOLISCH, R., and Schuman-Leclerq, F., Zur Frage der Kohlehydrattoleranz

der Diabetiker, Wien. klin. Woch., 1903, xvi, 1321-1323.
KtJLZ, R. E., (1) Beitrage zur Pathologie und Therapie des Diabetes mellitus,

Marburg, 1874.

(2) Klinische Erfahrungen tiber Diabetes mellitus, (Rumpf, AldehoflF,

Sandmeyer), Jena, 1899.

(3) Zur Prioritatsfrage bezuglich der Oxybuttersaure im diabetischen Harn,

Arch. exp. Path. u. Pharm., 1884, xviii, 290.
KussMAUL, Zur Lehre vom Diabetes mellitus, Deutsch. Arch. klin. Med., 1874,

xiv, 1-46.
Labbe, M., (1) Tol6rance comparee des divers hydrates de carbone par I'organ-

isnie des diabetiques, Bull, et mim. Soc. mid. Mp. Paris, 1907, xxiv,

221-234.

Ref. by L6pine
and Sauerbeck.

HISTORY 71

Labbe, M., (2) La cure de Mgumes sees chez les diabetiques, Bull, Acad, med.,
1914, Ixxi, 52-54.

(3) Die Diat beim Diabetes gravis, Med. Klin., 1913, ix, 1973-1978.

(4) Les cures de 16gumes sees dans le diabete, Rev. med., 1914, xxxiv,

473-503.
Lampe, E., Haferkuren bei Diabetes mellitus, Z. physik. u. diiUet. Therap., 1909-10,

xiii, 213-231.
Lampe, E., and Strassner, H., Blutzuckerwerte der verschiedenen Diatformen

bei Diabetes, Med. Klin., 1913, ix, 1462-1465.
Lancereaux, E., (1) Note sur un cas de syphilis pulmonaire,

suivie de reflexions sur la syphilis des visceres

et les erreurs dont elle est I'objet, Bull. Acad.

mid., 1877, vi, 1108-1120.

(2) Nouveaux faits de diabete sucre avec alteration du

pancreas, Ihid., 1888, xix, 588-609.

(3) Le diabete maigre: ses sympt6mes, son evolution,

son prognostic et son traitement; ses rapports
avec les alt6rations du pancreas. — fitude com-
parative du diabete maigre et du diabete gras,
Union Med., 1880, xxix, 161-167; 205-211. Lcfons
de clinique medicale (Review), /6«i.,1890, xiv,
439-441.

Lapierre, a., Sur le diabete maigre dans ses rapports avec les alterations du
pancreas, These de Paris, 1879. Ref. by Lepine and Sauerbeck.

Latham, J., Facts and Opinions concerning Diabetes, London, 1811.

Lemann, 1. 1., The Allen Treatment in Diabetes by Fasting, /. Am. Med. Assn.,
1915, Ixv, 2118.

Lenn£, a., (1) Wesen, Ursache, und Behandlung der Zuclierkrankheit, Berlin,
1898.

(2) Die Eiweisszufuhr in der Diabetesdiat, Verhandl. Cong. inn. Med.,

1900, xviii, 587-600.

(3) Ein weiterer Beitrag zur Diatregelung und medikamentosen Behand-

lung des Diabetes mellitus, Therap. Gegenw., 1907, ix, 251-255.
Leo, H., Ueber die Stickstoffausscheidung der Diabetiker bei Kohlehydratzu-

fuhr, Z. klin. Med., 1893, xxii, 225-244.
Lepine, R., (1) Le diabete sucre, Paris, 1909.

(2) Fortschritte in der Behandlung des Diabetes mellitus seit 50 Jahren,

Berl. klin. Woch., 1913, 1, 477-481.

(3) Progres de nos connaissances sur la pathogenic et le traitement du

diabete sucre et de I'acetonSmie, Rev. med., 1913, xxxiii, 449-473,
601-624, 769-783.
Levy, L. H., Diabetes. The Complications and Treatment; the Allen Plan,
N. Y. Med. J., 1915, cii, 1192-1195.

72 CHAPTER I

Leyton, O., (1) Discussion on the Treatment of Diabetes Mellitus by Alimentary
Rest, Proc. Roy. Soc. London, 1915-16, ix, Therap. and Pharm.
Sect., 63-76. Also 76-90, (Spriggs).

(2) The Treatment of Diabetes Mellitus by Alimentary Rest, Practitimer,

1916, xcvii, 24-43, 401-429.

(3) The Modem Treatment of Diabetes Mellitus, Brit. Med. J., 1917,

i, 252-^254.
LiPETZ, S., Ueber die Wirkung der v. Noorden'schen Hafercur beim Diabetes

melitus, Z. klin. Med., 1905, Ivi, 188-197.
LovEWELL, C. H., Modern Treament of Diabetes, Illinois Med. J., 1917, xxxi,

240-245.
Lrsz, G., (1) The Elements of the Science of Nutrition, Philadelphia, 2nd
edition, 1909; 3rd edition, 1917.
(2) Metabolism in Diabetes, /. Am. Med. Assn., 1910, Iv, 2105-2107.
Magendie, (1) Note sur la prfisence normale du sucre dans le sang, Compt.
rend. Acad., 1846, xxiii, 189-193; Gaz. mSd., 1846, 734-736, ref. Vogel,
J., Pathologic des Bluts, Canstatt's Jahresh., 1846, iii, 27.
Magnus-Levy, A., (1) Die Oxybuttersaure und ihre Beziehungen zum Coma
diabeticum. Arch. exp. Path. u. Pharm., 1899, xlii, 149-237.
(2) Diabetes mellitus, SpezieUe Pathologic und Therapie innerer Krank-
heiten (Kraus and Brugsch), 1913, i, Tl. 1, 1-85.
Mandel, a. R., and Lusk, G., (1) Diabetes Mellitus. — Report on a Case, Includ-
ing a New Method of Prognosis, /. Am. Med. Assn., 1904, xUii, 241.
(2) StofiEwechselbeobachtungen an einem FaUe von Diabetes mellitus, mit
besonderer Beriicksichtigung der Prognose, Deutsch. Arch. klin.
Med., 1904, Ixxxi, 472-492.
Marsh, H., Observations on the Treatment of Diabetes Mellitus, Dublin Quart.

J. Med. Sc, 1854, xvii, 1-19.
Marshall, M., The Starvation Treatment of Diabetes, /. Michigan Med. Soc,

1916, XV, 150-151.
Martin, C. F., and Mason, E. H., Observations on the Starvation Treatment of

Diabetes, Am. J. Med. Sc, 1917, cliii, 50-58.
McNabb, E., The Treatment of Diabetes after the Method of Allen, /. Ten-
nessee State Med. Assn., 1915-16, viii, 477-481.
Menke, J., Ueber das Verhalten des Blutzuckers bei Kohlehydratkuren und tiber
den Wert der Blutzuckerbestimmungen fur die Therapie des Dia-
betes, Deutsch. Arch. klin. Med., 1914, cxiv, 209-248.
VON Mering, J., (1) Ueber die Abzugswege des Zuckers aus der Darmhohle,
Arch. Physiol., 1877, 379-415.

(2) Ueber experimentellen Diabetes, Kong. inn. Med., 1886, v, 185-189.

(3) Behandlung des Diabetes mellitus und insipidus, Handbuch spez.

Therapie, Renzoldt and Stintzing, 1895, ii, 3te. Abt., 59-104.
VON Mering, J., and Minkowski, 0., Diabetes mellitus nach Pancreasexstirpa-
tion. Arch. exp. Path., u. Pharm., 1889-90, xxvi, 371-387.

HISTORY 73

M'Gregoe, R., Comparative State of Urea in Healthy and Diseased Urine, and
the Seat of the Formation of Sugar in Diabetes Mellitus, London
Med. Gaz., 1837, xx, 268-272.

MiALHE, L., (1) Apercu theorique sur la cause de la maladie d6signee sous le
nom de diab&te ou de glycosurie, Compt. rend. Acad., 1844, xviii, 707.

(2) De la digestion et de I'assimilation des matieres sucrees et amiloides,

Ibid., 1845, XX, 954-959.

(3) Traitement raisonne du diabete par les substances alcalines, /. mSd. et

ckir. prat., 1846, xvii, 23-24; Formule du traitement du diabete sucr6
par les substances alcalines, Ibid., 77-78; ref. Vogel, J., Pathologie
des Bluts, Canstatt's Jahresb., 1846, iii, 29.

(4) NouveUes recherches sur la cause et le traitement du diabete sucre ou

glucosurie. Bull. Acad, mid., 1847, xiii, 1224; Bull, therap., 1849,
xxxvi, 198-208. Ref. by Lepine.

(5) Nouvelle th6orie du diabete sucr6 ou glycosurie. Union Mid., 1866,

XXX, 218-221, ref. by Lepine; also Arch. gin. mid., 1866, i, 746.
MiALHE, L., and Contour, Observation d'un cas de diabete sucr6 traits et gueri

par I'emploi des alcalis et des sudorifiques, Compt. rend. Acad., 1844,

xix, 111-112.
Minkowski, O., (1) Ueber das Vorkommen von Oxybuttersaure im Ham bei

Diabetes mellitus. Arch. exp. Path. u. Pharm., 1884, xviii, 35-48.

(2) Nachtrag iiber Oxybuttersaure im diabetischen Harne, Ibid., 147-150.

(3) Untersuchungen iiber den Diabetes mellitus nach Exstirpation des

Pankreas, Ibid., 1892-3, xxxi, 85-189.

(4) Die neueren Anschauungen iiber den Diabetes mellitus, Med. Klin.,

1911, vii, 1031-1036. The Newer Opinions concerning Diabetes
Mellitus, translation by G. Lusk, Med. Rec, 1913, Ixxxiii, 220-225.

MosENTHAL, H. 0., The Treatment of Diabetes Mellitus in Dispensaries, Med.
Rec, 1915, Ixxxvii, 589-592.

Moses, H. M., The Present Treatment of Diabetes Mellitus, Med. Rec, 1916,
xc, 1069-1072.

MossE, A., La cure de pommes de terje dans les diabetes sucr6s et les compli-
cations diabetiques. Rev. mid., 1902, xxii, 107-121, 279-308, 371-
411, 620-658, 1098.

Naunyn, B., (1) Zur Pathologie und Therapie des Diabetes mellitus, Verhandl.
Cong. inn. Med., 1886, v, 183-184.

(2) Die diatetische Behandlung des Diabetes mellitus, Samml. klin. Vortr.,

1889, (Innere Medicin, No. 116), 3129-3168.

(3) Nephritis und Diabetes und Nierendiabetes, Z. prakt. Aerzie., 1898, vii,

525-530.

(4) Der Diabetes melitus, Deutsch. Klin., 1902, iii, 1-34.

(4A) Die Behandlung des Diabetes melitus, Deutsch. med. Woch., 1905,
xxxi, 977-982.

74 CHAPTER I

Naunyn, B., (S) Der Diabetes melitus, Vienna, 1906.

(6) Diatetische Behandlung der Glykosurie und des Diabetes, Z. artzl.

FortUld., 1908, v, 737-746.
Nesbitt, G. E., Remarks on the Alien Treatment of Diabetes, Dublin J. Med.

Sc, 1916, cxlii, 379-385.
Nicolas, and Gueudeville, V., Recherches et experiences medicales et chimi-

ques sur le diabete sucre ou la phthisurie sucree, Paris, 1803. Ref.

by Sauerbeck and others.
VON NoOEDEN, C., (1) Die Zuckerkrankheit und ihre Behandlung, Berlin, 6th
• edition, 1912.

(2) New Aspects of Diabetes, New York, 1912.

(3) Die Diat bei Diabetes gravis, Med. Klin., 1913, ix, 611-616.

Opie, E. L., (1) On the Relation of Chronic Interstitial Pancreatitis to the Islands

of Langerhans and to Diabetes Mellitus, /. Exp. Med., 1900-1901, v,

397-428.
(2) Diabetes MeUitus Associated with Hyalin Degeneration of the Islands

of Langerhans of the Pancreas, Bull. Johns Hopkins Hosp., 1901,

xii, 263-264.
Opplee, B., and KiJLZ, C., Ueber das Vorkommen von Diabetes mellitus bei

Ehegatten (Uebe'rtragbarkeit des Diabetes mellitus), Berl. klin.

Woch., 1896, xxxiii, 583-586, 612-615.
Paley, S. H., The Allen Treatment in Diabetes MeUitus, N. Y. Med. J., 1916,

ciii, 159-161.
Palmer, W. W., The Concentration of Dextrose in the Tissues of Normal and

Diabetic Animals, /. Biol. Chem., 1917, xxx, 79-114.
Palmer, W. W., and Van Slyke, D. D., Studies of Acidosis. IX. Relationship

between Alkali Retention and Alkali Reserve in Normal and Tatho-

logical Individuals, /. Biol. Chem., 1917, xxxii, 499-507.
Pavy, F. W., (1) Researches on the Nature and Treatment of Diabetes, London,

1862.

(2) The Physiology of the Carbohydrates, London, 1894.

(3) Carbohydrate Metabolism and Diabetes, London, 1906.
Petersen, V. C. E., Von der Wirkung der " Kohlenhydrattage" in der Dia-

betesbehandlung, Deuisch. med. Woch., 1912, xxxviii, 1276-1278.
von Petteneofer, M., and Voit, C, Ueber den Stoffverbrauch bei der Zucker-

harnruhr, Z. Biol., 1867, iii, 380-444.
Petters, W., Untersuchungen iiber die Honigharnruhr, Vrtljschr. prakt. Heilk.,

1857, iii, 81-94.
PiORRY, Sur un nouveau systeme de medication employe avec succes dans le

diabete sucre, Compt. rend. Acad., 1857, xliv, 133-134. (Abstract.)
PiSKATOR, O., Ueber den Erfolg der Haferkur bei Diabetes mellitus. Inaugural

Dissertation, Giessen, 1912.
Popper, M.^ Das Verhaltnis des Diabetes zu Pankreasleiden und Fettsucht,

Osterreich Z. prakt. Heilk., 1868, xiv, 193-196. Ref. by Sauerbeck.

HISTORY 75

Potter, N. B., Cure de jeflne d'Allen pour le diabete sucr6, Ann. mid., 1917,

iv, 341-374.
Prasad, K., Experiences in Diabetes Mellitus in the East, Seventeenth Inter-
national Congress of Medicine, London, 1913, vi (2), (Medicine),

327-332.
Prout, W., On the Nature and Treatment of Stomach and Renal Diseases,

London, 1848.
Rathery, M. F., (1) Les pommes de terre dans I'alimentation du diabetique,

Bull, et mem. Soc. mid. h$p. Paris, 1911, xxxi, 160-173.
(2) De I'alimentation parmentiere dans le diabete. La Clinique, 1913, viii,

770-773.
Ratjlston, B. O., and Woodyatt, R. T., Blood Transfusion in Diabetes Mellitus,

J. Am. Med. Assn., 1914, Ixii, 996-999.
Regnault, v., and Reiset, J., Recherches chimiques sur la respiration des ani-

maux des diverses classes, Ann. chim. et phys., 1849, xxvi, 299-519.

Ref. by Lusk.
Reicher, K., Verhandl. deutsch. Kong. inn. Med., 1913, xxx, 179.
Reynoso, a., Memoire sur la presence du sucre dans les urines, et sur la liaison

du phenomene avec la respiration, Ann. sc. nat., 1855 (Zoologie), iii,

120-153. Ref. by Lepine.
Richardson, W., Remarks on Diabetes, London, 1871.
Richartz, H. L., Kohlehydratkuren bei Diabetes, Deutsch. med. Woch., 1913,

xxxix, 650^652.
RoBBiNS, C. P., Observations and Experiences of the Allen Treatment, J. -Lancet,

1917, xxxvii, 300-302.
RoLLO, J., (1) An Account of Two Cases of the Diabetes Mellitus; with Re-
marks, etc., London, 1797. Ref. in texts.
(2) Cases of the Diabetes Mellitus, London, 2nd edition, 1798.
ROLLY, F., Zur Theorie und Therapie des Diabetes mellitus, Deutsch. Arch. klin.

Med., 1911-12, cv, 494-521.
RosENPELD, G., Ueber die Entstehung des Acetons, Deutsch. med. Woch., 1885,

xi, 683-685.
Roth, N., Ueber Mehltage bei Diabetes, Wien. klin. Woch., 1912, xxv, 1864-1868.
ROTJBITSCHEK, R., and Gaupp, 0., Die Kohlehydrattherapie des Diabetes, Med.

Klin., 1913, ix, 1038-1041.
RuMPE, T., (1) Ueber die Assimilationsgrosse und den Eiweissumsatz beim

Diabetes mellitus, Berl. klin. Woch., 1898, xxxv, 945-948.

(2) Ueber Eiweissumsatz und Zuckerausscheidung beim Diabetes mellitus,

Ibid., 1899, xxxvi, 185-189.

(3) Untersuchungen iiber Diabetes mellitus, Z. klin. Med., 1902, xlv,

260-313.
Salomon, M., Geschichte der Glycosurie von Hippokrates bis zum Anfange des
19. Jahrhunderts, Deutsch. Arch. klin. Med., 1871, viii, 489-582.

76 CHAPTER I

Sauerbeck, E., Die Langerhansschen Inseln des Pankreas und ihre Beziehung

zum Diabetes mellitus, Ergebn. dig. Path. u. path. Anal., 2te Abt.,

1902, viii, 538-697.
Saundby, R., Diabetes Mellitus, in Allbutt and Rolleston's System of Medicine,

London, 1908, iii, 167.
ScHiFF, J. M., Untersuchungen iiber die Zuckerbildung in der Leber,' und den

Einfluss des Nervensystems auf die Erzeugung des Diabetes, Wiirz-

burg, 1859.
ScHU-LiNG, Inaugural Dissertation, Leipsic, 1911. Ref. by Joslin (2) and by

RoUy.
ScmEOKAUER, H., Haferkur und Blutzuckergehalt bei Diabetes mellitus, Berl.

klin. Woch., 1912, xlix, 1129-1132.
ScHMiTZ, R., (1) 4 Falle von geheiltem Diabetes und kurze Bemerkungen iiber

die Entstehung desselben, Berl. klin. Woch., 1873, x, 211-214, 222-

224.
(2) Kann der Diabetes mellitus ubertragen werden? Ibid., 1890, xxvii,

449-451.
ScHNEE, E., Diabetes, Its Cause and Permanent Cure, 1889, translation by

R. L. Tafel.
Seegen, J., Der Diabetes mellitus, Leipsic, 1870.
Senator, H., Ueber das Vorkommen von Diabetes mellitus bei Eheleuten und

die Uebertragbarkeit des Diabetes, Berl. klin. Woch., 1896, xxxiii,

665-666.
Severin, Kohlehydratkuren bei Diabetes mellitus unter besonderer Beruck-

sichtigung des Blutzuckers, Berl. klin. Woch., 1912, xlix, 2010-2011.
Spriggs, E. I., (1) Discussion on the Treatment of Diabetes Mellitus by Ali-
mentary Rest, Proc. Roy. Soc. London, 1915-16, ix, Therap. and

Pharm. Sect., 76-90. Also 63-76, (Leyton).
(2) The Fasting Treatment of Diabetes, Brit. Med. J., 1916, i, 841-845.
Stadelmann, E., Ueber die Ursachen der pathologischen Ammoniakausscheidung

beim Diabetes mellitus und des Coma diabeticum. Arch. exp. Path.

u. Pharm., 1883, xvii, 419-444.
Staubli, C, Beitrage zu Pathologie und Therapie des Diabetes mellitus, Deutsch.

Arch. klin. Med., 1908, xciii, 107-160.
Stengel, A., Diabetes, Progr. Med., June, 1915, 393-407; June, 1916, 426-440.
Stengel, A., Jonas, L., and Austin, J. H., The Treatment of Diabetes Mellitus

with Special Reference to Allen's Method, Pennsylvania Med. J.,

1915-16, xix, 283-287.
Stetten, De W., The Conservative Treatment of Diabetic Gangrene of the

Lower Extremity, J. Am. Med. Assn., 1913, Ix, 1126-1133.
Stillman, E., The Fasting Treatment of Diabetes Mellitus, with Special Reference

to Acidosis, Am. J. Med. Sc, 1916, cli, 505-515.

HISTORY 77

Stillman, E., Van Slyke, D. D., Cullen, G. E., and Fitz, R., Studies of

Acidosis. VI. The Blood, Urine, and Alveolar Air in Diabetic

Acidosis, 7. Biol. Chem., 1917, xxx, 405-456.
SxoKVis, B. J., Zur Pathologie und Therapie des Diabetes naellitus, Deutsch.

Kong. inn. Med., 1886, v, 125-159.
SxROUSE, S., (1) Diabetes in the Young, Med. Clin. Chicago, 1916, ii, 2, 327-338.
(2) Inanition in the Treatment of Diabetes Mellitus, Ibid., 1917, ii, 5,

999-1006.
Thomson, R. D., On the Digestion of Vegetable Albumen, Fat, and Starch, The

London, Edinburgh and Dublin Philosophical Magazine, 1845, xxvi,

322-328, 418-424. Ref. by Pfliiger.
TiEDEMANN, F., and Gmelin, L., Die Verdauung nach Versuchen, Heidelberg

and Leipsic, 1826-27, i.
Trommer, Unterscheidung von Gummi, Dextrin, Traubenzucker und Rohr-

zucker, Pharm. Centr., 1841, 762-764.
Trousseau, A., Lectures on Clinical Medicine, translated from edition of 1868

by J. R. Cormack, London, 1869, iii, 491-527, Lecture Ixiv, "Glyco-
suria: Saccharine Diabetes."
Tyson, J., A Treatise on Bright's Disease and Diabetes, Philadelphia, 1881 and

1904.
Van Slyke, D. D., and Cullen, G. E., Studies of Acidosis. I. The Bicarbonate

Concentration of the Blood Plasma; Its Significance, and Its Deter-
mination as a Measure of Acidosis, J. Biol. Chem., 1917, xxx, 289-

346.
Van Slyke, D. D., Studies of Acidosis. II. A Method for the Determination of

Carbon Dioxide and Carbonates in Solution, J. Biol. Chem., 1917,

xxx, 347-368.
Van Slyke, D. D., Stillman, E., and Cullen, G. E., Studies of Acidosis. V.

Alveolar Carbon Dioxide and Plasma Bicarbonate in Normal Men

During Digestive Rest and Activity, J. Biol. Chem., 1917, xxx,

401-404.
Van Slyke, D. D., Studies of Acidosis. VII. The Determination of /3-Hydroxy-

butyric Acid, Acetoacetic Acid, and Acetone in Urine, /. Biol. Chem.,

1917, xxxii, 455-493.
Van Slyke, D. D., and Fitz, R., Studies of Acidosis. VIII. The Determination

of /3-Hydroxybutyric Acid, Acetoacetic Acid, and Acetone in Blood,

J. Biol. Chem., 1917, xxxii, 495-497.
Walter, F., Untersuchungen Uber die Wirkung der Sauren auf den thierischen

Organismus, Arch. exp. Path. u. Pharm., 1877, vii, 148-178.
Warren, P., Two Cases of Diabetes Mellitus Treated with Opium, Med. Tr.

College Phys. London, 1813, iv, 188-225.
Waters, E. E., The Treatment of Diabetes by Alimentary Rest, Indian Med.

Gaz., 1917, Hi, 42-46.

78 CHAPTER 1

Watt, R., Cases of Diabetes, Consumption, etc., with Observations on the His-
tory and Treatment of Disease in General, Paisley, 1808.
Weichselbaum, a., (1) Ueber die Veranderungen des Pankreas bei Diabetes

mellitus, Sitzungsb. kais. Akad. Wissensch., 1910, cxix, 73-281.
(2) Ueber die Veranderungen des Pankreas bei Diabetes melitus, Wien.

klin. Woch., 1911, xxiv, 153-159.
Weichselbaum, A., and Stangl, E., (1) Zur Kenntnis der feineren Veranderungen

des Pankreas bei Diabetes mellitus, Wien. klin. Woch., 1901, xiv,

968-972.
(2) Weitere histologische Untersuchungen des Pankreas bei Diabetes

mellitus, lUd., 1902, xv, 969-977.
Weiland, W., Kohlehydratkuren und Alkalitherapie bei Diabetes mellitus; ihre

Indication und Prognose, Z. exp. Path. u.. Tkerap., 1912-13, xii,

116-151.
Weintraud, W., Untersuchungen iiber den Stoffwechsel im Diabetes mellitus

und zur diatetichen Therapie der Krankheit, Bibliotheca medica,

1893, Abt. D', No. I.
Werbitzki, F. W., Zur Frage des Einflusses der verschiedenen Kohlehydrate auf

die Glykosurie der Diabetiker, Z. exp. Path. u. Therap., 1909, vi,

235-253.
Williams, J. R., Recent Studies in Diabetes Mellitus, N. Y. Slate J. Med.,

1916, xvi, 412-418.
Williamson, R. T., (1) Diabetes Mellitus and Its Treatment, Edinburgh and

London, 1898.

(2) On the Treatment of Diabetes Mellitus with Casein and Cream, Brit.

Med. J., 1915, i, 456-458.

(3) The Treatment of Diabetes Mellitus, Lancet, 1917, i, 650-652.
Winternitz, W., and Strasser, A., Strenge Milchkuren bei Diabetes mellitus,

Centr. inn. Med., 1899, xx, 1137-1139.
WoLE, L., and Gutmann, S., In welcher Weise wirken Diatkuren auf das Ver-

halten des Blutzuckers bei Diabetikern? Z. klin. Med., 1914, Ixxix,

394^420.
Wolfe, W., Ueber Mehlkuren und Kartofielkuren bei Diabetes, If ed.^/iw., 1913,

ix, 789-790.
Woodyatt, R. T., (1) Prepared Foods and Diabetic Articles, Illinois Med. J.,

1909, xvi, 666-674.

(2) Discussion, Tr. Assn. Am. Phys., 1915, xxx, 339-340.

(3) Am. Sac. Advancement Clin. Investigation, 1915, Abstract of Proceed-

ings, 25-28.
ZiMMER, K., (1) Ein Beitrag zur Lehre vom Diabetes mellitus, Deutsch. Klin.,
1867, xix, 127-128, 133-136, 149-152, 160-162.

(2) Die nachste Ursache des Diabetes mellitus, Ihid., 1871, xxiii, 41-42.

(3) Der Diabetes mellitus, sein Wesen und seine Behandlung, Leipsic, 1871.

(4) Die Muskeln als Quelle des Zuckers im Diabetes mellitus, Deutsch.

Klin., 1873, xxv, 61-62.

CHAPTER II.
GENERAL PLAN OF TREATMENT.

This chapter, like the later ones, aims only to present the methods
and experience of the present investigation. A multitude of ques-
tions and details concerning the treatment of diabetes must neces-
sarily be left to general text-books on the subject. Discussion of the
observations and suggestions of others who have used this treatment
must also for the most part be omitted in the interests of brevity.
For details of the laboratory methods employed, reference may be
made to the original papers or to the excellent description in Joslin's
text-book.

As emphasized from the outset, every case of diabetes must be
managed according to its own requirements, and the best results are
obtainable only when the treatment is intelhgently individualized.
At the same time, a basic plan is essential, inasmuch as one general
principle underhes the treatment of all cases, and organization and
routine conduce to both ease and efl&ciency. The system developed
in this hospital may be described under the following headings:

I. General measures.

II. Treatment up to cessation of glycosuria in simple cases.

III. Complications and emergencies (acidosis, infections).

IV. Treatment following cessation of glycosuria.
V. Ideals of diet and laboratory control.

VI Practical management of diets.

79

I. General Measures.

A. The Routine Care of Patients.

1. Hospital Observation.^AH. the cases treated have been under
direct hospital observation. Between February 24, 1914, and July
1, 1917, altogether 96 patients were received, for a total of 165 ad-
missions, an average of 1.72 admissions to each patient. The great-
est number of admissions for a single patient was five. The total
number of days of diabetic treatment was 11,308, giving an average
of nearly 69 days to each admission. The longest single admission
was 304 days, the shortest a few hours (acute death). Hospital ob-
servation has seemed advisable for the following reasons: (a) to obviate
possible danger from acidosis during the active treatment of the dis-
ease by the fasting method; (b) to govern with the greatest possible
accuracy the individual diet, while the preliminary tests of tblerance
are being made, a ration built up, and its suitability demonstrated;
(c) for the instruction of the patient, in order that he may carry out
his diet and tests properly after leaving the hospital.

2. Confinement to Bed. — ^Unless made advisable by some complica-
tion or by a dangerous degree of acidosis, the patients have not been
confined to bed. Even during the most trying period of treatment,
namely the initial fast, it has not been uncommon for patients to lessen
the tedium of treatment by going to theatres, concerts, etc.

J. Clothing. — ^As many patients show a decided susceptibility to
cold weather, they have been advised to dress wannly, but without
specific instructions. The use of exercise, as discussed in Chapter V,
has obviated this condition to some ^tent, especially for that great
majority of diabetic cases which rank as relatively mild. But the
extremely low diets required for the very severe cases provide so
little combustible material that body heat must be conserved as care-
fully as possible.

4. Baths. — It has not been attempted to gain effect through hydro-
therapy. Bath temperature has been left to individual inclination.
Patients with severe diabetes have naturally chosen warm water.

80

GENERAL PLAN OF TREATMENT 81

5. Catharsis. — Chronic and obstinate constipation has been a rule
with few exceptions in the past history of these as of other severely
diabetic patients. It was regulated by cathartics before bran was
incorporated into the dietary of the hospital. This and the bulky
vegetables have almost banished constipation. When something
more active has been needed, the usual cathartics (castor oil, salts,
cascara sagrada) have been employed.

6. Medication. — The principle has been followed of giving drugs
to diabetic patients only as they would be used for other persons. No
medicines have been employed with a view to influencing the dia-.
betes, and no effect upon the diabetes has been observed from any of
those employed for incidental purposes. The recommendations of
various drugs in the past have probably been based upon inadequate
control and study of the cases. Special mention may be made of the
dangerous possibilities of anesthetics, especially chloroform. It is well
known that drugs of the chloroform class most easily injure the liver
when it is poor in glycogen. The visceral disturbances set up by
general anesthesia readily explain the production of either glycosuria
or acidosis, as so frequently described. The dangers are greatest
where the treatment is poorest, and the majority of diabetics under
thorough treatment are able to undergo suitable anesthesia without
glycosuria and without dangerous acidosis.

7. Complications. — The experience with these has not been large.
It is discussed in Chapter VII and in the individual case histories.
The treatment of the acute forms is described under Section III of
the present chapter. Metabolic complications in general do not in-
terfere with the treatment of the diabetes; the present diabetic diet
does not conflict, for example, with the usual treatment of nephritis.
In regard to infectious complications, it may be said that the ideal of
treatment is to make the patient as nearly like a normal person as
possible by means of diet, and then to use as nearly as possible the
measures considered best for normal persons. The recently debated
question of the relation of infections, sometimes focal and minor in
degree, to the etiology of diabetes is discussed in Chapter VIII.
Certainly bad tonsils, teeth, and other foci are sources of injury for
diabetic patients, which in acute attacks often give rise to glycosuria
and acidosis, and which may interfere seriously with the success of

82 CHAPTER II

dietetic treatment. It has been the policy with this series of cases to
have teeth or tonsils removed or other operations performed on the
same basis as advised for normal persons by conservative specialists.
Experience has indicated that such measures are beneficial from the
standpoint of the general health and also of the diabetes, in obviating
chronic and acute disturbances and the downward progress associated
with them. No patient has died or suffered harm from such opera-
tions performed while on the dietetic treatment, and it appears that
there is less danger from performing needed surgery than from
omitting it. On the other hand, if toxic absorption causes diabetes,
evidently the damage has mostly been done before the case has come
under treatment, for in no instance has the removal of a focus of in-
fection been followed by cure of the diabetes or by improvement
beyond that seen in other patients.

B. Ward Regulations and Clhstical Remarks.

1. Respiration, pulse, and temperature have been recorded at 4
hour intervals when fever was present or when acidosis or other
crisis threatened. Otherwise they have been taken every 12 hours.
Sohie of the information which may be gleaned from these signs in
diabetic patients follows.

Respiration. — Increased breathing is one of the classical indications
of acidosis, the increase generally applying to both volume and fre-
quency. Ordinarily it is a fairly constant and rehable index of danger,
unless obscured by the use of alkali; but in the type of acidosis pro-
duced by fasting, it may, like the drowsiness and other symptoms,
be far less prominent than in typical diabetic coma.

Pulse. — It may some day be possible to analyze the records of
these cases with respect to the pulse rate. F. G. Benedict has noticed
a relation between pulse and metabolism, and he and Joshn reported
acceleration of the pulse in proportion to increased metabolism in
severe cases of diabetes with active symptoms present. Patients in
the present series entering the hospital with intense diabetes and
threatening acidosis have regularly shown rapid pulse, which has
become slower under treatment. A few examples appear in tables in
certain of the case histories. Marked bradycardia has been observed

GENERAL PLAN OF TREATMENT 83

in some of the patients subjected to extreme undernutrition and the
corresponding reduction of metabolism, but this has not been con-
stant. The conditions are evidently not simple. On the one hand,
the tachycardia out of proportion to any possible exaggeration of
metabolism in impending coma is clearly an effect of intoxication upon
the circulation. On the other hand, Dr. Alfred Cohn has observed
in radiograms of some of these emaciated patients a diminution of the
cardiac shadow even out of proportion to the thinning of the chest.
This wasting of the heart muscle, like other states of general or circu-
latory weakness, might of itself alter the rate, especially in the di-
rection of tachycardia. With the uncertainty concerning the re-
spective influence of metabohc and other factors, a uniform inter-
pretation may be difficult.

Temperature. — It being understood that the temperature of diabetic
patients typically is normal, notice should be taken of variations in
two directions. Elevation of temperature often accompanies severe
acidosis, as illustrated in a few of the case records in this series.
Otherwise, fever of any grade generally points to infection, and ceases
with the finding and removal of the cause. Subnormal temperature
■^is common in proportion to malnutrition, whether the latter is due
to failure of assimilation of food with active diabetes, or to thera-
peutic restriction of diet. In the most severe cases of this series under
treatment, the rectal temperature has commonly been below 98° and
above 96°F. An important practical point is to watch the tem-
perature when children must be subjected to extreme xmdernutrition.
Even though the weakness is not visibly graver than before, a fall of
temperature to the neighborhood of 96-95°F. is a signal of danger,
which generally comes in time to permit warding off death by giving
food. If acidosis or stubborn glycosuria makes a full diet inad-
visable, even protein alone may support strength to the point where
fasting can be continued. More careful attention to this point
might possibly have prevented the fatal collapse which occurred in
several children of this series. The low temperatures in severely
diabetic patients are readily explained by the failure to receive or to
assimilate (according to the treatment) enough combustible material.
The same circxunstance may wholly or partly explain another im-
portant clinical phenomenon, namely the absence or diminished grade

84 CHAPTER n

of the febrile reaction to infection in some cases. Joslin called atten-
tion to the possibility of an almost complete lack of symptoms with
tuberculosis, even in an advanced stage. Something similar may be
witnessed occasionally with other infections. Either the weakened
individual is deficient in reactive power, or possibly the resultant of a
subnormal temperature and a febrile tendency may be something like
a normal temperature. This possible fallacy regarding fever should
be borne in'mind, and if a patient under rigid dietary control begins
to do badly without apparent cause, careful search should be made
for the infection which is often responsible.

2. Blood Pressure. — ^Aside from extraneous causes of hypertension,
the blood pressure of diabetic patients is generally normal or below
normal. Not only weakness, but also the intoxication of acidosis, is
responsible for the depression. Several patients received in extreme
stages have had a systolic blood pressure below 80, and in certain
others the circulation was so feeble that it was not possible to deter-
mine the pressure accurately. In such cases the question always arises
whether the patient can endure the week or more of absolute fasting
required to control his diabetes. In actual fact, every adult has
passed successfully through such fasting, not only without collapse,
but generally with more or less gain in strength, as indicated for one
thing by a rise in blood pressure. It thus appeared that intoxication
was the most dangerous factor in the depression, and relief from it
even at the price of fasting was necessary to save life. Therefore a
dangerously low blood pressure is not necessarily any contraindication
to fasting. On the other hand, it is possible that a fall in blood pres-
sure during fasting or extreme imdemutrition may be a signal of
danger, but the clinical observations have not been sufl&cient to show
whether this is a reliable warning or whether it comes in time to per-
mit of averting the danger.

3. Body Weight. — AU patients have been weighed naked each morn-
ing after voiding urine and before breakfast. The weight has been
recorded in kilograms. The weight is very valuable among the cri-
teria of treatment, though it is well known to be only a crude measure
of the true body mass. Patients with intense active diabetes some-
times seem to be dried out by diuresis; they may hold or gain weight
by water retention during fasting and for days or weeks on inadequate

GENERAL PLAN OF TREATMENT 85

diet thereafter. Fall in weight is sometimes sudden, to the extent of a
kilogram or two on a fast-day, without evident significance. Fat diet
following carbohydrate diet gives rise to such a water loss. The
commonest cause of precipitous fall in weight for a series of days is
acidosis. This melting away of weight and strength is seen in its
most alarming degree in the occasional cases combining intense acido-
sis, maximal D:N ratio, exaggerated nitrogen loss, and, with these,
rapid water loss. The opposite condition of sudden gain in weight
represents water retention, sometimes associated with relief from
glycosuria or acidosis, or with carbohydrate feeding, but frequently
from obscure cause. Even without nephritis, it is commonly con-
nected with salt retention and removed by salt-free diet. It may
differ in degree at different times and especially in different patients,
from invisible storage to extensive edema. Edema, sometimes huge,
has been well known in connection with the large salt intake in "oat-
meal cures," and especially with high dosage of sodium bicarbonate.
In Joslin's experience, water loss is one of the most dangerous, and
water retention or edema one of the most favorable conditions when
combating a dangerous acidosis. On the other hand, the more severe
cases have the greatest tendency to edema. This edema may there-
fore be classed among the indications of severity, though not aU
severe cases show the tendency equally. Apart from any mere
changes in the function of the kidney for salt, it is likely that there
is some unknown metabolic cause affecting the general tissues, either
belonging in some measure to diabetes itself, or perhaps largely or
wholly a phenomenon of undernutrition. It may possibly belong in
a series of dropsical conditions due to malnutrition, a related member
being the "hunger swelling" ^ of the wretchedly poor classes in Poland
on an almost exclusive potato diet in the present war, another re-
presentative being the "epidemic dropsy"^ of famine times in India,
another being the edema of cachectic children, while at the farther
extreme is beri-beri.

^Budzynski, B., and Chelkowski, K., abstracted in /. Trop. Med., 1916, xix,
141-42.

^Megaw, J. W. D., Indian Med. Gaz., 1910, xlv, 121; /. Am. Med. Assn.,
1911, Ivii. 826.

86 CHAPTER n

4. Measurement of Fluids. — It is well known and has lately been
emphasized by DuBois that an accurate water balance is one of the
hardest of all things to determine. In our cases the fluid intake and
output have been measured daily, and occasionally gross retention
or loss of water has been thus demonstrated. The information
afforded is necessarily vague and inaccurate. No allowance was made
for the water content of foods, and especially the large quantities of
vegetables generally given made this unknown factor a considerable
one. Most of the apparent discrepancies of intake and output
shown in the graphic charts are thus explained.

(a) Intake. — Thirst is not of abnormal degree in ordinary
diabetic patients under proper treatment, one of the advantages of
which is the relief from the discomfort of polydipsia and the incon-
venience of polyuria and nycturia. Severely diabetic patients on
very low diets generally drink rather freely, merely for the sake of
something to fill the stomach. There has been no need to restrict
fluids, except temporarily in a single patient (No. 1) who had formed
the habit of excessive drinking, and in a few others during periods of
marked edema. There is also no need to urge drinking of mineral
waters or anything else under the conditions of proper diet, there
being no poisons to wash out of the system. This may be an im-
portant advantage in cases with a complicating nephritis, with lim-
ited ability to excrete fluid. The one emergency which demands the
forcing of fluids to capacity is dangerous acidosis, as mentioned later
in this chapter.

(b) Output. — If an occasional patient drinks so little that the urine
is unduly concentrated, a troublesome turbidity may cloud the sugar
reactions; and instead of using chemical reagents for clearing, the best
plan all around may be to urge the patient to drink a normal quantity
of water. Usually in the severe cases the urine is very pale and clear,
both because of the excessive drinking stimulated by hunger and be-
cause of the small total content of solids. It thus resembles in appear-
ance the traditional diabetic urine, but a sharp difference is found in
the very low specific gravity. Delicate sugar reactions are easily
seen. The total 24 hour urine is saved in four separate portions each
day, the divisions coming at mealtimes. During all the earlier and
greater part of the investigation, days were counted from 7 a.m. of

GENERAL PLAN OF TREATMENT 87

one day to the same hour the next day. More recently, for general
hospital convenience, a change has been made to the less commenda-
ble method of counting from midnight to midnight. Accordingly
at present the order of periods is as follows:

Period I. Midnight to 7 a.m.
Period U. 7 a.m. to 11:30 a.m.
Period III. 11:30 a.m. to 5:30 p.m.
Period IV. 5:30 p.m. to midnight.

Two considerations favor this latter plan, namely that all urine is re-
corded under the date on which it was voided instead of being dis-
tributed over two dates, and second that the separation of days is
made at a time when there is little work in the hospital instead of at
the busy hour of 7 a.m. The arguments against this plan and in
favor of the former plan are more weighty, first that patients are sub-
jected to the inconvenience of being wakened at midnight to void
urine, and second that the urine of a day does not correspond cor-
rectly to the diet of the day, inasmuch as the break between days is
made at a time when the digestion of the last meal is not finished.
The segregation in four periods has a decided value. Patients are
not free from glycosuria unless the test is absolutely negative in every
period. Even when the reaction seems negative in the mixed 24
hour urine, tests of the separate specimens may show not only the
presence of faint traces but also after which meal they appeared.
Also a transgression of diet is sometimes revealed by a marked reac-
tion occurring suddenly in some period and clearing up thereafter,
whereas a slight reaction in the mixed 24 hour urine might be of doubt-
ful interpretation.

5. Meals. — Food has generally been served in three meals, with
sometimes an additional lunch at bedtime. In the past, minor pecu-
liarities in the relation between meals and glycosuria have been de-
scribed, generally glycosuria after carbohydrate ingestion and clear-
ing up during the night, more rarely glycosuria only at night, absent
during the day perhaps because of exercise. Also, it seems a promis-
ing plan to give carbohydrate distributed in nmnerous small fractions
at intervals, or in slowly digestible form, so as to avoid flooding

88 CHAPTER II

the system suddenly; and from such work as that of Thomas,'
it might appear that the best assimilation of protein would be ob-
tainable by the same scheme. Undoubtedly it is possible to flood the
system, especially with a quickly absorbable carbohydrate such as
sugar, when the same quantity in divided doses would be assimilated
without glycosuria. But under the ordinary conditions of diabetic
treatment, the essential cause back of either regular or irregular
glycosuria is a diet in excess of the tolerance or a persistently high
blood sugar. As for distribution of foods between meals, a mild case
of diabetes on a proper diet should be independent of such variations
within limits of reason. With severe cases, the difficulty lies in the
persistence of the hyperglycemia set up by either carbohydrate or
protein, so that before the effect of one ingestion has subsided the next
is superimposed upon it. In general, the total diet is the important
thing, and httle is to be hoped from unusual fractionation. A ration
so close to the verge of tolerance as to require such aid will not be
permanently tolerated. On the other hand, when the blood sugar
is kept normal by a total diet truly within the assimilative power,
glycosuria or other trouble does not result from any arrangement of
meals that is likely to be made.

6. Regulation of Habits. — Precision regarding diet has been the
chief essential. In other matters, it seems advisable, in brief, that
patients should do whatever is necessary to maintain the best possible
general health, while restraining their activities within the limits set
by their diet and tolerance. With a more hopeful general prognosis,
it becomes highly important to guard patients against alcohol and
drug habits; and especially as opium and other drugs are worthless
or harmful, and alcohol as a means of adding calories is also inadvis-
able, it is important that their widespread use in diabetic treatment
be stopped. With other indulgences, such as tobacco, tea, and coffee,
there are two opposite considerations. On the one hand, these articles
in excess probably injure all persons, and even in moderation appar-
ently injure some persons. On the other hand, the diabetic is denied
so many enjoyments in diet that it is a pity to deprive him of any
pleasures unnecessarily. Accordingly, the patients have been enjoined

* Thomas, K., Arch. Physiol, 1910, 249-285.

GENERAL PLAN OF TREATMENT 89

to use such moderation in these respects as is advisable for normal
persons. Smoking within careful limits has seemed very enjoyjtble
to men long addicted to it. All habitual users of coffee have derived
the utmost comfort from it, especially during fasting. From one to
three cups a day has been the allowance, and decaffeinized coffee has
been used if there was any suspicion of harm. In all other matters,
the usual life of the patient should be altered just as little and just as
much as demanded by the particular case. It will be seen that fre-
quently in this series men have continued business, children have at-
tended school, and everything possible has been done to keep patients
contented and useful. Especially those with milder diabetes are able
to pursue practically a normal existence with care only in diet, and
this fact is one of the most hopeful elements in the prognosis and one
of the greatest encouragements to fidelity in diet. Either mental or
physical overstrain is injurious to such a degree as to be out of the
question for the severest cases and inadvisable even for the milder
ones. Healthful rest, short of ennui, is important. Exercise is dis-
cussed in Chapter V. While reduction of weight and diet to a cer-
tain point is known to be compatible with physical and mental
efl&ciency, with more extreme diminution these are progressively im-
paired, until in the severest cases emaciation and invahdism are
chronic. Even in these worst cases, much depends on the individual
disposition, and light emplojonent or amusement aids in keeping the
mind off the subject of food. If it comes to a choice, neurasthenia is
preferable to overfeeding. Finally, one of the most important points
in the hygiene of diabetics is the avoidance of infections, either great
or small. This need not contraindicate outdoor exercise in cold
weather, which may be one means of building up resistance for pa-
tients who can stand it. For some, however, it means avoiding
crowds or any places where colds or influenza may be caught. For
others, it means the removal of foci of chronic or recurrent infection,
even at the risk involved in surgery. The best possible care of the
teeth, skin, and body in general is advisable at all times, though the
extreme susceptibility of diabetics to troubles from these sources is
greatly diminished under proper diet.

II. Treatment up to Cessation of Glycosuria in Simple Cases.

Any fixedly prescribed routine is opposed by the necessity of indi-
vidualizing treatment to suit the special needs of every case, and by
the desirability of free play for the physician's individuality and ad-
justment to environment. The basic principle of undernutrition
being grasped, the application can be made in various ways. This
period is occupied by the observation diet (if used) and the initial
fast.

A. The Observation Diet.

All sorts of possibilities are of course open in the choice of an ob-
servation diet. One conservative plan is to leave the patient for a
short time on as nearly as possible the same diet he has been taking,
to guard against the danger of any sudden change, especially in the
form of carbohydrate reduction. In order to establish data for com-
paring cases with one another and also with cases in the literature
treated by older methods, the majority of patients in this series have
been placed for a few days (2 to 5) on a diet somewhat as follows:

Protein per 24 hrs.

Carbohydrate per 24 hrs.

Fat per 24 hrs.

1.5 gm. per kilo.

10 to 25 gm.

Sufficient to bring total calories to 35 per
kilo body weight.

This is essentially the traditional "carbohydrate-free diet," for the
low carbohydrate allowance is given only in the form of green vege-
tables, such as have usually been included in diets of this description
in the past. With close laboratory and clinical observation, no hesi-
tation has been felt in placing patients abruptly on this diet; and
even though this was done in some very severe cases, such as No. 8,
the ability to control acidosis when necessary by fasting prevented any
mishap. This plan was necessary for the accurate study of the earlier
cases. Also, it frequently shortened the requisite period of fasting,

90

GENERAL PLAN OF TREATMENT 91

when the previous diet had been grossly improper. In general, it is
not therapeutically advisable, and was seldom used when the pa-
tient's condition at entrance seemed dangerous. More recently, this
observation period has been omitted, treatment has been begun im-
mediately, and the severity of the diabetes has been judged by the
subsequent progress and food tolerance.

B. The Initial Fast.

If diabetes is deficiency of the function of food assimilation, logi-
cally the most effective method of relieving strain upon this function
should consist in withholding food. The benefit of such relief should
apply not only to glycosuria but also to acidosis, irrespective of
whether the latter is wholly secondary to glycosuria or is partly a
specific diabetic phenomenon; and the slight ketonuria developed by
normal persons on fasting should not serve to confuse this expectation.

With regard to the initial tests on dogs, it may be mentioned that
irregularities in the glycosuria following total pancreatectomy are
well known, and in particular the urine may become free from sugar
just befort death from starvation or weakness; but the fatal diabetic
cachexia is always present and freedom from glycosuria never avails
to save the lives of such animals. Also, partially depancreatized dogs,
of the type best suited for therapeutic experiments, in the severest
stage continue to show glycosuria through the most prolonged fast-
ing, up to death or the hopeless exhaustion just preceding death. It
was a serious question whether the severest clinical cases are in a
similarly hopeless state, or whether they still correspond to the type
of dogs which can be freed from glycosuria by fasting and then kept
symptom-free at a more or less reduced weight by suitable regulation
of the total diet. Some encouragement was found in the results of
the shorter therapeutic fasts employed by former writers, but there
was nowhere in the literature any description of such a procedure as
contemplated, or any information as to what might happen if a pa-
tient with the worst type of diabetes were suddenly subjected to abso-
lute fasting until sugar-free. Accordingly, as noted in the history
of patient No. 1, the first attempt was made with considerable caution.
It so happened that this patient, although of the type in which glyco-

92 CHAPTER II

suria and acidosis had formerly been viewed as hopeless, and though
chosen as one in whom at least no great harm could be done, re-
sponded with rather exceptional ease to this treatment, and both
glycosuria and sjonptoms of impending coma quickly disappeared.
If this first experience had concerned a case, such as frequently en-
countered later in the series, requiring from a week to 10 days for
sugar-freedom, it is a question whether courage would have held out;
and if by any chance this first case had been one of the rare ones which
develop fatal acidosis on fasting, the proposed treatment might have
ended there. The first fact demonstrated was that even the severest
cases of human diabetes almost invariably become free from glycosuria
and as a rule also improve markedly as respects acidosis upon fasting.

Regarding the practical carrying out of the initial fast in ordinary
cases, the following details may be noted.

Water. — It is advantageous on general principles that the total
daily intake of fluids be at least 1500 to 2000 cc, and patients have
therefore been encouraged to drink tap water or any kind of mineral
or table water rather freely. In hot weather, cracked ice has some-
times been rehshed. No limit is placed on the fluid intake if patients
desire more than the above quantity.

Alcohol. — The use of alcohol was one of the early precautions
adopted to support strength during fasting. According to some earlier
literature, it not only produced no glycosuria but also might diminish
acidosis. In a number of cases, 50 to 350 cc. whisky or brandy
were given daily, in small divided doses every hour or two, the limit
for any individual being always short of producing subjective or ob-
jective symptoms. A rather general misapprehension was created
by the first papers pubhshed, as it was not clearly understood that
the use of alcohol was not new but was adopted entirely from pre-
vious writers, that it was used for cases with extreme weakness or for
other special purposes, and that it was never a primary or essential
feature of the treatment. Experience has tended to discredit it even
for the purposes for which it was first employed. It is a decided com-
fort during fasting to persons already habituated to its use. In other
persons, especially women and children, it often excites discomfort
or even nausea, and is therefore detrimental. It has an unmistakably
bracing action in weak patients, but its real effect is probably more

GENERAL PLAN OF TREATMENT 93

harmful than beneficial. Soup and coffee are preferable in almost
every case.

Soup. — In the great majority of cases, clear meat soup has been
allowed in quantities up to 600 cc. daily during fasting. The trivial
quantities of protein contained are harmless, but even such can be
avoided if desired by substituting beef extract. Soup is very com-
forting, and the fluid and salts may be valuable.

Coffee. — One to three cups of coffee or Kaffee Hag daily are pleasing
and supporting to most fasting patients. It is not advisable to
cultivate the coffee habit in children or other persons not addicted
to it.

Solids. — Three to six of the bran muffins described subsequently in
this chapter have generally been allowed daily during fasting. They
are of some use in diminishing the feeling of emptiness. Theoreti-
cally, small quantities of thrice cooked vegetables might be permissi-
ble in the milder cases, but have very seldom been used, because there
is no use in trying to trick the appetite too far, and it is better for
patients to learn to bear rigorous fast-days.

Purgation. — The habitual constipation of most diabetics renders a
cathartic advisable at the outset. With the use of bran, there is
generally more natural tendency to defecation. On a prolonged fast
with only fluid intake, the patient may safely go for a week or more
with no bowel movement. There is no specific virtue in purgation.

Edema. — ^As mentioned, water retention even to the point of visible
edema is sometimes observed in fasting, especially in the more severe
cases. It seems never to have been reported in normal persons on
simple fasting, but only in connection with prolonged malnutrition
and abnormal living. Diabetics vary in susceptibiUty, but the imme-
diate cause of edema is usually the salt of the above ingesta, especially
the soup. No harm has ever been observed from the fluid retention.
The prevention or remedy consists in the restriction or exclusion of
salt.

Comfort and Strength. — Fasting, sometimes up to a month or more
in duration, has been a well known practice for purposes of metabolic
studies and sometimes for public exhibitions, and the subjects have
retained physical and mental powers through these long periods and
have denied any real suffering. Fasting has also been one of the com-

94 CHAPTER n

monest religious customs of numerous peoples and sects. On the other
hand, the omission of a single meal is often felt as a great privation,
and a few days' abstinence from food is viewed as something serious
and alarming, not only by people in general but even by numerous
physicians. The most profoundly emaciated and cachectic diabetic
patients undergo even a 10 day fast with ease and safety. The re-
fusal of a patient to undergo fasting is generally as much the fault
of his physician as of himself, provided he is of a type who
will faithfully carry out any kind of careful dietetic treatment. The
first fast generally dispels the dread, and furthermore is valuable for
discipline.

As described in the histories, the fasting treatment has been applied
to patients in all physical states, from those appearing in full health
and strength to those seeming at the point of death from weakness and
emaciation. The effect upon the immediate comfort has varied with
individuals. Some patients have entered with nausea or vomiting
which prevented eating; others rejoiced in quick relief from acidosis
symptoms; others had been overfed till fasting was agreeable in itself.
At the other extreme are the occasional patients who, whether in
good or poor health and flesh, feel weak, uncomfortable, and depressed
whenever they fast. In the intermediate position are the great ma-
jority of patients, who find fasting more or less inconvenient but no
serious hardship, and who carry on their usual activities or amuse
themselves in various ways during either long or short fasts. As
stated elsewhere, some very weak patients have unmistakably gained
strength on fasting. More or less decline in strength is the rule.
Even in the most extreme cases, no adults have died from weakness
either during or within any short time after fasting to sugar-freedom.
Two small children (cases Nos. 45 and 71) entered with such a com-
bination of extreme diabetes, acidosis, and weakness that the choice
between coma and starvation could not be avoided; and it is conceiv-
able that such a dilemma may be possible in very rare adult patients.
The use of levulose as a restorative in sudden collapse of strength is
illustrated in cases Nos. 4 and 45.

Laboratory Control. — ^Laboratory tests are qualitative and quanti-
tative. So much information is derivable from the former that it is
generally possible to carry through a fast successfully by their guid-

GENERAL PLAN OF TREATMENT 95

ance alone. The qualitative test for urinary sugar has been the key-
stone of the plan, since fasting is terminated on the day after it
becomes negative. Acidosis can also be judged fairly safely by the
increase or diminution of the ferric chloride test of the urine and of the
Rothera test applied to the blood plasma (Wishart),and by the acid or
alkaline reaction of the urine; by simply noting the dosage of alkali
required to turn the urine alkaline, the latter test acquires a quantita-
tive significance Also, in default of accurate measurements of blood
alkalinity, the test proposed by Yandell Henderson* should not be
overlooked; namely, that normal persons can hold the breath 30 or
40 seconds without specially deep preparatory inspiration, but that
this period diminishes somewhat in proportion to the reduction of
blood alkali.

Of quantitative tests, that for blood sugar is of minor practical im-
portance during the fast. Generally the blood sugar falls; sometimes
it rises at first even when glycosuria is diminishing and the general
condition improving; and in the rare cases where fasting results badly,
the persistence or increase of hyperglycemia may be one significant
feature; but other tests are more important danger signals. Also,
the quantity of sugar excreted in the urine is of little practical im-
portance in the great majority of cases, though persistence or increase
of glycosuria gives warning of the failure of fasting, and likewise of
the danger of coma even independently of direct acidosis tests.

Quantitauve nitrogen determinations are of significance for the ra-
pidity of protein destruction and the D : N ratio, which is an im-
portant index of severity. Increase of the quantity of amino-acids in
blood and urine also marks the severe cases.

Possibly some significant behavior of the blood fat may later be
found, but at present such analyses have no established value as a
guide for treatment at this stage. In dogs it seems probable that
fasting acidosis is sometimes accompanied by increased lipemia, but
in human patients fasting generally produces no increased turbidity
of the plasma.

The essential danger that threatens during fasting is acidosis, there-
fore the tests for it are preeminent. All analyses of the urine are un-

* Henderson, Y., /. Am. Med. Assn., 1914, Ixiii, 318.

96 CHAPTER n

reliable. Very high excretion of acetone bodies is dangerous, but yet
the progress may be favorable; while lower excretion may indicate
either less acidosis or more dangerous retention. The urinary am-
monia is governed not only by the degree of acidosis but also by
other factors such as the total nitrogen output and the alkali dosage.
The recently developed blood tests are the most convenient as well
as the most trustworthy. The Van Slyke method' of determining
the C02-combining power of the blood plasma has been used in the
present series of cases, because of its combination of ease and accu-
racy. Methods showing the carbon dioxide tension of the alveolar air°
are simple and almost equally reliable. Those requiring the patient's
cooperation encounter difficulty in coma or similar states, and even
the bag or mask methods are subject to possible errors from circulatory
or other causes. The air analyses are specially useful to those de-
siring to avoid the taking of blood, but both physicians and patients
should learn that blood ought to be taken for various analyses as a
means of intelligent diabetic treatment. The hydrogen ion concen-
tration of the blood, determined by either the gas-chain method, the
oxyhemoglobin dissociation, or the more convenient procedure of Levy,
Rowntree, and Marriott,' has recently attracted attention clinically as
well as experimentally, but is not so early or delicate an indicator of
danger as the CO2 capacity. Quantitative analyses for acetone bodies*
in the blood may sometimes be of practical service. For example, if
high and increasing, they may give warning of impending coma, even if
this is not revealed by any of the above mentioned tests. On the
other hand, the danger in different diabetic cases by no means runs
parallel to the ketonemia, neither has any infallible index yet been
derived from the relative proportions of /3-oxybutyric and acetoacetic
acids.

In summary, therefore, all laboratory tests are open to more or less
fallacy. The more tests performed, the more easily and accurately
can the condition be judged and needful measures instituted. If it

6 Van Slyke, D. D., and CuUen, G. E., J. Biol. Chem., 1917, xxx, 289.
^ Fridericia, L. S., Bed. klin. Woch., 1914, li, 1268. Marriott, W. M., J. Am.
Med. Assn., 1916, Ixvi, 1594.

' Levy, Rowntree, and Marriott, Arch. Int. Med., 1915, xvi, 389.
* Van Slyke and Fitz, J. Biol. Chem., 1917, xxxii, 495.

GENERAL PLAN OE TREATMENT 97

comes to a question of the absolute minimum of laboratory work on
which fasting can justifiably be conducted, the methods of choice are
the Benedict qualitative sugar test for the urine and the Van Slyke
determination of the bicarbonate reserve of the blood plasma, together
with the nitroprusside reaction in the plasma.

III. Emergencies and Complications.

A long list of greater or lesser troubles associated with diabetes
might be enumerated here. As mentioned in Chapter VII, the pres-
ent experience indicates that these traditional complications, which
have been the cause of so much suffering and fatality in diabetes, are
for the most part avoidable under efficient treatment; and when al-
ready present, it is beUeved that the best and quickest means of
curing any of these or hindering their further advance lies in fasting
followed by restriction of the total diet as described. A physiological
condition which stands as a real complication in the management of
diabetes is pregnancy. It was encountered in only one instance in
this series, namely case No. 38, where it was associated with a hope-
less complex of infections. JosUn's experience has proved that the
formerly grave prognosis for both mother and child can now be much
brighter; and unless deterred by eugenic considerations, the possi-
bility exists for women with not too severe diabetes to go through
pregnancy successfully. The essential requirement is the same
thorough dietetic treatment as for other patients. By far the chief
emergencies or complications, however, which are liable to be en-
countered in undertaking the fasting treatment, are acidosis and
infection.

A. Acidosis.

1. Definition.

If the normal resting metabolism upon which calorimetric studies
are based be accepted as a standard, acidosis may be broadly defined
as any departure from this normal tending to turn the reaction of the
body to acid. It may thus include all possible states of increased
production or deficient destruction of acid, administration of acid,
retention of acid, or deficient supply or abnormal loss of bases. The
most important clinical type of acidosis is a ketosis; namely, the
occurrence of abnormal quantities of the so called acetone bodies —

98

GENERAL PLAN OF TREATMENT 99

whether due strictly to excessive formation or deficient utihzation is
uncertain. Therefore, in accordance with Naunyn's dictum, acidosis
is present in diabetes whenever an abnormal increase of acetone sub-
stances is demonstrable in the urine or blood. Attempts to replace
this metabohc or biological definition by purely chemical conceptions
of alteration of reaction, derived from experiments in vitro, have
thus far been scientifically fallacious, on grounds which need not be
reviewed here, and clinically are open to the following objections:
(a) these changes represent no independent phenomenon, but only
some late stage of a process which should properly be regarded as a
unit from beginning to end; (6) the striking abnormal production of
acid in the protoplasm, perhaps up to 100 gm. of /3-oxybutyric acid
daily, is the essential disorder to be defined, and the mere neutraliza-
tion of the products by alkali cannot properly be regarded as abolish-
ing this biological acidosis; on the contrary, the necessity of amimonia
formation or alkah dosage to maintain neutral relations should in it-
self be considered evidence of acidosis; (c) the therapeutic point of the
whole matter is that attempts to treat by neutrahzation of products
are often illusory and sometimes dangerous even as temporary meas-
ures, and lead always to failure in the end, while successful treatment
can only consist in stopping the abnormal acid production which is
the essential disturbance.

2. Fasting and Undernutrition Txeatment in Various Types.

The ordinary acidosis of severe diabetes is no contraindication to
beginning a fast, and, as already stated, typically diminishes pro-
gressively during the fast. The more severe the acidosis, and the
more imminent the impending coma, the more urgently is fasting de-
manded, so that the patients of this series who have entered in the
most dangerous condition have been placed immediately on strict
fasting. The results have been favorable, as shown in Chapter VII.

In the milder cases of diabetes, including those previously free from
acidosis, some degree of ketonuria, generally shght, sometimes rather
heavy, may develop during fasting, without danger or any need for
changing the fasting program. Exceptionally, however, in cases in-
herently either mild or severe, blind persistence in fasting may result

100 CHAPTER II

in dangerous or fatal acidosis, as happened in one case (No. 30) in the
present series. This difficulty, though exceptional, is certain to be
encountered if any considerable nimiber of cases are treated; and the
fact that it had not formerly been known is one evidence of the
newness of the fasting method.

This atypical behavior may sometimes be expected in middle-aged
or elderly patients, who have carried their diabetes for possibly 5
to 15 years with little or no apparent harm, whose glycosuria may be
heavy or moderate, whose acidosis may be chronic but slight, and
whose bodily state may be that of good nutrition or slight obesity.
Such a case may appear very promising for quick and gratifying re-
sults. During the fast, glycosuria may persist or diminish; keto-
nuria is generally qualitatively heavy, but quantitatively may not
be great, especially if alkali is not given. What is seen clinically is
first a vague malaise, often with headache or pains elsewhere, dizzi-
ness, and increasing prostration. Nausea seems to be invariable, and
the gravest stage is when vomiting is established. Though the con-
dition is acidosis, the appearance is not that of t3^ical coma.
Dyspnea may not be prominent, and the consciousness may be clear
up to the last hours or minutes of lif^. The end comes with uncon-
trollable vomiting and profound and rapidly progressive weakness.

Treatment in this final stage offers little hope. Glucose or levulose,
orally, rectally, subcutaneously, or intravenously, should theoretically
be most important, provided the diabetes is inherently mild enough to
permit any effective utilization. A few patients elsewhere are said
actually to have been saved by such means. If food can be taken at
all, whatever protein-carbohydirate diet promises to be best retained
is indicated. The use of sodium bicarbonate is customary; it is prob-
ably best given intravenously, possibly by rectum, to avoid nausea.
If carbohydrate or protein as above described succeeds in arresting
the underlying intoxication, it is possible that the cautious use of
bicarbonate may guard against death from simple deficit of alkali
and thus .may be a temporary assistance in tiding over the crisis.
The traditional large doses of alkali are dangerous. If the other
measures fail to arrest the underlying toxic process, alkali, in any
dosage is useless, and the patient dies just as certainly whether the
blood alkalinity is low or high.

GENERAL PLAN OF TEEATMENT 101

The essential treatment lies in prevention, and with simple care
these unnecessary accidents can be avoided. For this purpose, Joslin
has introduced a precautionary program, which, briefly, consists first
in omitting fat from the diet, then gradually diminishing protein and
finally carbohydrate, down to complete fasting unless glycosuria ceases
before. This is opposite to the orthodox treatment of a few years ago,
which started with a gradual reduction of carbohydrate. The plan
is theoretically sound, embodying the same general principle of under-
nutrition which underlies all this treatment. Besides the usual loss
of a little time, there is an imaginable disadvantage in very rare cases,
which might be controllable by immediate fasting but within a few
days might be advanced past hope; also it is a possible question
whether a threatening acidosis may ever be aggravated by food of
any sort, even protein and carbohydrate. The only concrete ob-
servation is in case No. 55 of this series, where it must be confessed
that the diet which made trouble on November 5 did contain an
appreciable quantity of fat. In favor of the gradual procedure are
the following considerations: first, in Joslin's experience, which is
larger than any other, dangers such as here suggested have not actu-
ally been met; second, the duration of the initial fast is shortened;
and third, the occurrence of fasting acidosis has been entirely pre-
vented. This modification has therefore been widely adopted and
will doubtless continue in extensive use. Though Joslin's own cases
are studied by complete laboratory methods, the modified treatment
becomes more important in proportion as laboratory control is lacking.

As already stated, the method of immediate fasting has been em-
ployed in the whole of the present series. Since the early experience
(case No. 30) calling attention to the occasional danger, it has been a
simple matter by combined clinical and chemical observation to avoid
further mishaps. The practical management of dangerous cases of
acidosis may be discussed according to the three classes into which
they fall.

(a) Typical Coma. — ^Patients in actual deep coma generally die.
The considerable proportion of recoveries in this series shows that
treatment is not entirely useless. With coma impending but not yet
complete, death was the usual outcome under former methods, but
under fasting treatment the usual outcome is recovery. It is be-

102 CHAPTER II

lieved that immediate fasting, with the adjuvants mentioned below,
is the safest general rule for cases of threatened coma. Generally the
improvement is quick, and may be evident within twenty-four hours
or less. Sometimes the patient may appear more stuporous on the
second day than on the first, and the blood alkalinity may be almost
stationary or may even fall a little. In all the favorable cases seen,
there has been unmistakable improvement by the third day. It is
worth noting that cases of ordinary coma, coming on in the usual
manner on any kind of diet, have never shown injury from fasting;
i.e., fasting acidosis has not developed where the threatened coma was
due to feeding. The patients whom inexperienced physicians are
likely to be afraid to fast are the ones who usually need fasting most
and who usually show the most striking benefits.

(&) Fasting Acidosis. — ^As stated, occasional patients, in no imme-
diate danger of coma on whatever diet they may be taking, react to
fasting with an increase of acidosis, sometimes to dangerous degree.
The reason for this pecuharity is unknown, and there is also no known
way of foreteUing which cases will exhibit it. Examination of the
case records in this series will show that neither the mildness or severity
or duration of the diabetes, nor the initial degree of acidosis, nor the
intensity or persistance of glycosuria, nor the store of reserve fat
represented by obesity or emaciation, nor the supply of circulating
fat as represented by lipemia, necessarily stands as a determining
factor. The same patient at different times may behave oppositely.
Thus, several cases in this series displayed more or less tendency to
fasting acidosis at first, while at subsequent periods they reacted to
fasting with the usual decrease of acidosis. The essential treatment
for fasting acidosis is food; and the only known rule of procedure up
to the present is if a patient develops acidosis on feeding to fast
him, and if he develops acidosis on fasting to feed him. The kind of
food seems to be of subordinate importance. Thus the fasting acido-
sis symptoms of patient No. 35 ceased entirely on an orthodox protein-
fat diet, which represents the surest means of producing acidosis in
most patients. Nevertheless, it should not be considered that the
choice of diet is immaterial. Fat is theoretically disadvantageous.
Carbohydrate may be beneficial if the diabetes is not too severe, but
should be closely lunited to avoid too great hyperglycemia and gly-

GENERAL PLAN OF TREATMENT 103

cosuria. Protein is on general principles the most valuable food, and
either alone or with such carbohydrate as may seem advisable, it
makes up a low caloric diet which both relieves fasting acidosis and
at the same time continues the benefit of undernutrition. After a
few days of feeding, a second fast is generally well borne, and both
glycosuria and acidosis are brought under control as usual. After
thorough and successful treatment, all patients become able to
undergo fasting without danger from acidosis.

(c) Indistinctly separated from the above two groups are the occa-
sional examples of extraordinary intensity. Some cases of diabetes
almost from the outset, and others after a longer or shorter course of
ordinary symptoms, reach this degree characterized by maximal dex-
trose-nitrogen ratios, enormous protein breakdown, high amino-acid
values in blood and urine, and extremely threatening acidosis. Unless
further improvement in the treatment is devised, probably a majority
of such patients will continue to die, as did several in the literature,
and patient No. 39 in the present series. Some of them apparently
represent a degree of diabetes which is uncontrollable by fasting,
perhaps because fasting is not sufficiently potent to check the rush of
metabolism. There are three favorable considerations in regard to
this condition: first, though famiHar in dogs, it is rare in human pa-
tients; second, it is sometimes controllable by skillful treatment;
and third, a distinction exists between intensity and severity, for
if it is possible to weather the immediate storm of symptoms, these
extremely intense cases sometimes turn out later to be less severe
than anticipated. Thus, the patient of Geyelin and DuBois gained
a tolerance running into hundreds of grams of carbohydrate, and the
patient of Jonas and Pepper seemingly recovered from his diabetes
altogether. In Chapter VIII it is shown that the distinction rests
upon the apparently functional nature of the chief disturbance un-
derl3dng the intense symptoms, while anatomic destruction of the
islands of Langerhans, which is the fundamental basis of true severity,
has not necessarily advanced very far in these cases. As regards
acidosis, it may be assumed as a general principle that if fasting does
not control glycosuria the result will be coma. These cases differ from
those of group (b), which somehow react unfavorably to fasting irre-
spective of the presence or absence of glycosuria. The fatal acidosis

104 CHAPTER n

from prolonged fasting in the present group seems to occur only be-
cause of the persistence of high glycosuria. Successful treatment has
consisted in replacing fasting by an undernutrition diet of carbo-
hydrate or protein. Carbohydrate may be helpful for diuresis, but
with a maximal D:N ratio its value otherwise is questionable.
Protein offers theoretically the greatest advantages, in that it fur-
nishes carbohydrate and urea for diuresis and ammonia for neutral-
izing acids, and at the same time is the most important food for
maintaining strength and protecting body nitrogen. Successful
treatment with carbohydrate and protein is illustrated by the cases
of Geyelin and DuBois and Jonas and Pepper above mentioned.
Success with pure protein diet is illustrated by case No. 37 in this
series. This boy had first entered the hospital with impending coma
which had developed on a mixed diet and which cleared up smoothly
on fasting. In a relapse 11 months later, he was readmitted with gly-
cosuria which had resisted 8 days of fasting and acidosis which
threatened early coma if fasting were continued. By a practically
pure protein diet for 10 days, the acidosis and other symptoms were
relieved, and then glycosuria was easily abolished by fasting. As
mentioned, in some cases fasting, feeding, alkali, and all other measures
are unavailing, and here death occurs from acidosis or exhaustion
within a few days. Obviously, all cases of this group should be under
the care of the most experienced specialist available.

3. Adjuvant Measures and Remarks.

(o) Emptying Alimentary Canal. — ^When it is known that food has
been recently eaten, lavage of the stomach is advisable in impending
coma, and if there is any doubt, it is a wise precautionary measure.
Joslin makes it a routine for children with dangerous acidosis. It is
also important to empty the intestine thoroughly by a combination
of any vigorous purgative and high colonic irrigation. There may be
some incidental benefit from absorption of saline solution if this is
used for the colonic injections, or of. alkali if the irrigation is per-
formed with sodimn bicarbonate solution. Case No. 25 illustrates
the great difl&culty of securing adequate intestinal evacuation in some
instances, and also its importance.

GENERAL PLAN OF TREATMENT 105

(b) Drugs. — Except in accidental emergencies, it is doubtful if drugs
ever rescue patients from acidosis. Such an emergency is shown in
case No. 11. This patient was not actually saved; but if there is
cardiac and renal failure along with acidosis, it is evidently possible
that life may be preserved by medicines which restore circulation and
excretion. When any patient is sinking into. the stupor of ordinary
coma or the weakness of fasting acidosis, there is always the incli-
nation to stimulate heart, brain, and kidneys by such drugs as caf-
feine and digitalis, if only in the hope of supporting strength until
other measures have time to take effect. The liberal use of coffee, as
illustrated in a few cases in this series, may be of some slight service.
But whether employed early or late, drugs are probably never able to
change the result in uncomplicated cases. • If a large dose of alkali is
given intravenously, there is a possible question whether some circu-
latory stimulant might be of value for guarding against the sudden
death which sometimes follows within a few hours.

(c) Sugars. — Glucose and levulose have received long and extensive
trial as weapons against acidosis in the past. Their promise of use-
fulness is greatest in fasting acidosis, at the stage when all ordinary
food is vomited. They may then be given, preferably in 5 per cent
solution, rectally, subcutaneously, or intravenously. For the latter
purpose, a slow continuous infusion by some such device as that of
Woodyatt' appears obviously best. For ordinary coma, sugar might
have some value as a diuretic, and also for diminishing the formation
of acetone bodies if it can be burned. But as a rule, the blood sugar
is already undesirably high, and little if any sugar can be metab-
olized. It is well known that the attempted sugar treatment of coma
has in general been such a failure that it has been abandoned by the
best authorities. Von Noorden^" found absolute fasting more effective
than levulose, milk, or oatmeal for coma. Anything that aggravates
the diabetes and delays the clearing up of glycosuria may possibly
act injuriously also upon the acidosis. For these reasons it is be-
lieved that as a rule sugar or carbohydrate should not be used for the
treatment of ordinary cases of acidosis.

' Woodyatt, /. Biol. Chew,., 1917, xxix, 355-365.
'" von Noorden, C, Zuckerkrankheit, 1912, 388.

106 CHAPTER n

{d) Alcohol. — So far as observable empirically, alcohol has shown
no specific value in connection with acidosis. Some experiments to be
published later agree with the finding of Higgins, Peabody, and Fitz"
that it tends rather to increase acidosis. One objectionable feature
is its frequent nauseating effect. For these reasons, the use of
alcohol is considered inadvisable even for weak patients with serious
acidosis.

(e) Salts. — The value of inorganic salts and the danger of extreme
loss of salt have been emphasized especially by Joslin. Sodium
chloride is valuable as a diuretic; also, its retention is associated with
edema, and only one patient with edema in Joslin's experience has
ever died in diabetic coma. Therefore sodium chloride may be ad-
ministered by mouth in quantities up to 20 or 30 gin. daily unless
prevented by nausea or other contraindication; physiological saline
solution also is useful, by rectum, subcutaneously, or intravenously,
for conveying salt as well as fluid. In case No. 1 and a few others,
trial was made of giving also salts of potassium, calcium, and mag-
nesium, with a view to physiological balance, but no apparent advan-
tage has been found in this plan over the use of sodium salts alone.
Soup is valuable partly for the salts it contains.

(f) Fluids. — As already mentioned, the conduct of fasting with
ordinary moderate acidosis calls for only moderate quaritities of
hquids. On the other hand, the largest practicable fluid supply is
one of the most essential matters in the treatment of threatened
coma. Authorities from Rumpf to Joslin have recognized the
danger of desiccation of the body, especially with the vomiting which
occurs so frequently. The further use of fluids is to promote the
freest possible diuresis. Joslin set the standard of 10 liters a day
when possible. If the patient can drink and retain sufficient liquid,
it need not be given in other ways. The patient should be persuaded
to take water as much and as often as possible, either hot or cold, and
free use should also be made of coffee, tea, soup, cracked ice, or what-
ever else will aid in introducing fluid and perhaps also in preventing
nausea. If drinking is insufficient — for example, if an adult with im-
pending coma cannot retain 5 liters per day — recourse may be had to

" Higgins, H. L., Peabody, F. W., and Fitz, R., /. Med. Research, 1916, xxxiv.
263-272.

GENERAL PLAN OF TREATMENT 107

corresponding quantities of 0.85 per cent sodium chloride solution by
rectum, subcutaneously, or intravenously. From 500 to 1000 cc.
salt solution at a dose intravenously is considered by Joslin often
preferable to alkali, because less dangerous. Here again the Wood-
yatt injection apparatus might be advantageous. The reasons for
the importance of keeping up copious diur-esis by fliiids are the fol-
lowing. First, the possible concentration of acetone bodies in the
urine is limited (the highest observed by Fitz was between 9 and 10
gm. per liter); for this reason the excretion can often be multipHed
by almost as much as the quantity of urine is multiplied, and large
quantities of dangerous material thus removed. A high excretion,
e.g. 50 gm. or more of total acetone bodies daily, is never possible ex-
cept with abundant diuresis. Second, /3-oxybutyric and acetoacetic
acids circulate in the blood only in the form of salts. They are partly
eliminated as salts, but also to an important extent the kidney saves
the base for the body and excretes the free acids. Through this saving
of base by the acid-secreting power of the kidney, the administration
of fluid is equivalent in some degree to the administration of alkali,
without the special disadvantages or dangers of the latter.. .

(g) Laboratory Guidance. — Mention has already been made of the
various routine tests for acidosis, and preference expressed for the
Van Slyke plasma bicarbonate method. More reliance can be
placed upon the blood alkalinity, determined by this or by one
of the less direct methods, than upon any other single feature of the
condition, and without this information it is often impossible in
critical cases to judge progress or direct treatment intelligently.
With any serious degree of acidosis, estimation of the bicarbonate
reserve should be made once daily. In acute danger, such analyses
are sometimes demanded at frequent intervals, perhaps once every 4
hours, to indicate whether the response to treatment is favorable or
whether a change should be made. At this stage, the greatest service
of this test is to give warning of an increase of acidosis on fasting,
often before clinical symptoms make this evident, and in time to avert
the danger by giving food. As an arbitrary ground plan for apply-
ing the results of this test, the scheme in Table I may be suggested.
Nevertheless, clinical judgment and experience are important in
deciding whether unfavorable progress calls for a reversal of treatment

108

CHAPTER II

or for more rigorous adherence to the same plan. There is ample
evidence in the present series of cases that neither this nor any other
single test can be followed blindly as an infallible guide. Irregularities
are sometimes marked, even in absence of extraneous modif)dng factors.
Thus, patient No. 63 showed the lowest CO2 capacity in the entire
series (12.3 per cent), yet recovered promptly, whereas other patients
died although their bicarbonate reserve was by no means so low.
Patient No. 35 developed malaise, nausea, and drowsiness on fasting,
and the observers were convinced that unless fed he would have died
in the typical intoxication. The CO2 capacity was within normal
limits even without alkah dosage. Probably it would have fallen
at a later stage; but the significant facts are that the clinical symp-
toms alone gave warning in time to permit effective treatment, that

TABLE I.

Degree of acidosis.

Plasma COj.

Further drop of COz pennitted before interrupting fast.

vol. per cent

—

Above 53 .

To 45 volume per cent.

Mild.

53-40

Drop of 10 to 5 volume per cent.

Moderately severe.

40-31

(t (c 3 <( 2 " " "

Severe.

Below 31.

Fast interrupted in 6 to 12 hrs. unless CO2 rises
with fasting and alkali.

theintoxication symptoms increased when sodiumbicarbonateproduced
an actual rise in the CO2 curve, and that feeding cleared up the sjonp-
toms even though the CO2 capacity was slightly lower on certain subse-
quent days than at the time of the intoxication. Such discrepancies and
irregularities, spontaneous in origin, are much less numerous than those
resulting from alkaU therapy. Thus in case No. 30, a typical ex-
ample of acidosis with fatal result on fasting, the plasma bicarbonate
was forced up within normal limits by alkali dosage while well marked
intoxication was present, and the last reading, with severe and hope-
less intoxication existing, was 45 per cent, which falls within the limits
of "mild" acidosis according to the above table. Patient No. 45
had before admission been kept saturated with huge doses of sodium
bicarbonate. He' entered almost in coma, typical except, for absence
of hyperpnea, notwithstanding the CO2 capacity of 73.5 volume

GENERAL PLAN OF TREATMENT 109

per cent in his plasma. In full coma on September 9, the CO2 ca-
pacity was 84.9 volume per cent, i.e. abnormally high, and higher than
on other occasions without coma. Patient No. 71 was received in
coma with the usual low plasma bicarbonate of 22.1 per cent. On
the subsequent days he remained intoxicated and delirious, even
when the plasma bicarbonate was forced as high as 50.2 per cent,
which is near the normal level for a boy of 9 years. Thereafter it
was never below 38.8 per cent, and on the day of death in coma was
48.5 per cent. Patients not in this series have also been seen, who
died in coma notwithstanding normal CO2 capacity of the plasma.
These facts cast no reflection upon the accuracy of the analytical
method, but merely illustrate that dearth of alkali is not the sole nor
essential feature of the condition. Fasting is sometimes beneficial
even when the blood alkalinity falls somewhat; but in particular, a
high alkalinity is no a:ssurance of safety in the presence of obvious
chnical intoxication or a high and increasing concentration of acetone
bodies in the blood.

(h) Alkali Therapy. — This subject is partly discussed in connection
with the results of the treatment of coma, in Chapter VII. The pos-
sible benefits consist in relieving a dangerous dearth of alkali, and in
facilitating the elimination of acetone bodies. The possible harm lies
chiefly in the nausea which may result from oral administration and
the sudden death which may follow within a few hours after excessive
intravenous doses. It is conceivable that alkali may affect the toxic
state for either good or ill in ways not now understood. Both bene-
ficial and injurious effects are illustrated in the present series of
cases.

Close observation also shows that, whether the differences are sig-
nificant or accidental, the condition called diabetic coma does not
present a uniform picture. Aside from the rather atypical fasting
form, there are differences in the symptoms which usher in coma. At
one extreme are patients with extreme dyspnea, gasping so that
speaking and swallowing are difficult, yet with consciousness perfectly
clear until near the end. Such air-hunger is accounted for largely
though not entirely by acid intoxication, and alkali may perhaps save
life. Of patients of this tj^e, No. 63 was saved by alkali even after
he had gone on into unconsciousness, when he might not have been

no CHAPTER n

saved by simple fastingj^ the dyspnea of No. 39 was somewhat re-
lieved by alkali, but nevertheless she went on into stupor and died.
At the other extreme are cases characterized chiefly by malaise,
drunkenness, and drowsiness, with hyperpnea little marked; and these
prodromal symptoms may also be relieved by alkali, sometimes with
surprising promptness. The great majority of cases represent a
mixture falling between these two extremes."

The older clinical literature seems to prove that many patients with
continuous ketonuria were saved from both dyspnea and intoxication
for considerable periods by alkaU, and the onset of coma thus de-
layed. In the treatment of actual coma, alkaH has been seldom
successful, and the patients saved by it are few. Under all circum-
stances, its effect is necessarily temporary and palliative. The fact
is well known that the death rate from coma was not appreciably
altered by the introduction of the alkali treatment. If death was
somewhat deferred, the patient died subsequently in coma neverthe-
less. Magnus-Levy recognized that this result could be prevented
only by some method which would check the process of acetone body
production. Fasting checks this process; accordingly the great ma-
jority of cases of acidosis can be treated by this means alone, and
alkali holds no more than a minor adjuvant position. Its use has
seemed valuable under two conditions. The first is in combating a
long and stubborn acidosis, as in patient No. 23, both for relieving
malaise due to acidosis and for avoiding more serious danger. Ex-
perience does not prove whether it is best given in smaller doses, 5
or 10 gm. daily, for longer periods, or in larger doses on occasional
days when demanded by clinical or laboratory indications. Such a
need is rather rare, and the indiscriminate or routine use of alkali
is not to be recommended. Particularly prolonged administration,
of 2 weeks or more continuously, is probably best avoided, for fear of
harm in some patients. The second use of alkali has been for com-
bating coma in certain cases as already mentioned. Under all cir-
cumstances, it must be understood that control of the metabolic
condition by fasting or food is the essential means of treatment;

"^^This was written before reading the closely similar observations of Cam-
midge, Am. Med., 1916, xxii, 363-373, who suggests that one form is due to loss
of blood alkaU, the other to loss of tissue alkali.

GENERAL PLAN OF TREATMENT

HI

failure in this attempt must end fatally in spite of any dosage of
alkali, and the crisis is not past until the production of acetone bodies
is markedly and progressively diminishing.

In any of the three types of acidosis above described, continuously
high or increasing ketonemia and intoxication lead sooner or later
to a condition where the further administration of alkali is ineffec-
tual. The reason for the failure is unknown, because the real nature
of the intoxication is unknown. The possible irregularities in the
ketonemia and the alkaline reserve are indicated by observations of
Fitz'^ upon three fatal cases of coma (Table II).

TABLE II.

1st observation

, in early coma.

Interval
between 1st

and 2nd
observations.

Sodium
bicarbonate
by mouth
in interval.

2nd observation shortly before
death in coma.

Case No.

CO2 capacity
of plasma.

Total acetone

bodies of plasma

(as acetone)

per 100 cc.

CO2 capacity
of plasma.

Total acetone

bodies of plasma

(as acetone)

per 100 cc.

72 ■

71

sol. per cent
18.9
14.0
22.1

mg.

71.2 .

54.5
83.8

35 hrs.
8 "
8 days

gm.

0

25

72

per cent
26.7
17.0

48.5

mg.
127

97.8
192.5

By reference to the history of case No. 71, it will further be seen
that during 4 days before the final observation, the CO2 capacity
of the plasma ranged from 38.8 to 50.2 per cent, and the total acetone
of the plasma between 212.5 and 368.4 mg. per 100 cc. Also, there
was no constant relation between plasma alkali and plasma acetone.
These cases afford additional illustrations of increasing intoxication
and death notwithstanding rising alkaline reserve of the plasma.
Still other examples might be gathered from the literature to show
that the intoxication is by no means in proportion to the concentration
of total acetone in the plasma. Hence the failure of alkaU is not
necessarily an insufficiency of diuresis resulting in retention of these
acids or their salts. There is no evidence that alkali either increased
or diminished the production or accumulation of acetone bodies at
this stage. This point deserves further investigation. The sugges-

'^ Fitz, R.. Acetone Bodies in the Blood in Diabetes, Tr. Assn. Am. Phys., 1917,
xxxii, 155-158.

112 CHAPTER n

tion, especially of recent English authors," that the explanation hes
in different relative proportions of acetoacetic and hydroxybutyric
acids, the one being more toxic than the other, lacks proof at present.
There is need of more clinical observations and animal experiments
also on this question. In fact, nothing more than a descriptive status
is really estabhshed even for the word "intoxication." Diabetic coma
is a profound breakdown of metabolism. It may well be, in accord
with Woodyatt's ideas, that the abnormality extends through the
whole chain of intermediary compounds, that no one substance will
be demonstrable in lethal quantity and toxicity, but that the general
disorder of protoplasmic chemistry may be responsible for death.
Alkali could necessarily have little influence here. Certainly the con-
dition is complex. Ketonuria, ketonemia, lowered plasma alkalinity,
and clinical symptoms are ordinarily associated in a relation regarded
as t)^ical. The abnormahties of kidney function with severe acidosis
are notorious; they presumably involve variable excretion of acids and
bases; they necessarily upset any calculations based on normal renal
activity; and they may explain more or less of the exceptional behavior
noted. Aside from the occasional spontaneous variations, it is ob-
viously possible to distort the usual relations by artificial alteration of
one feature, for example raising the blood alkali by administration of
alkali, without altering the underlying process or the clinical result.
For practical purposes, sodium bicarbonate is the alkali of choice,
on the basis of effectiveness and innocuousness. A salt of strongly
alkahne reaction, such as sodium carbonate, deranges the stomach
more readily, and its intravenous use involves greater danger of
thrombosis in veins'^ or, in case of leakage, necrosis about them.
Stronger alkalies must be changed immediately into sodium bicarbon-
ate in the circulation, by chemical laws and because an actually alka-
line reaction of the blood would be incompatible with Kfe. This fact
does not necessarily conflict with Murlin's" observation of a differ-
ence in the action of sodiimi carbonate and bicarbonate upon experi-

1* Cf. Hurtley, W. H., Quart. J. Med., 1916, ix, 301-408. Kennaway, E. L.
Biochem. J., 1914, viii, 355-365.

" Cf. Umber, Deutsch. med. Woch., 1912, xxxviii, 1403.

" Murlin, J. R., and Sweet, J. E., /. Biol. Chem., 1916-17, xxviii, 261-288.
Murlin, J. R., and Graver, L. F., Ibid., 289-314.

GENERAL PLAN OF TREATMENT 113

mental animals; but no superiority of strong alkalies in the practical
treatment of human cases has been established. Any special advan-
tages in the use of other bases (potassium, calcium, magnesium) have
also not as yet been demonstrated.

Sodium bicarbonate can be given by the four usual routes.

By Mouth. — This method is preferred when possible. The maxi-
mar dosage is generally 2 or 3 gm. an hour or 5 gm. every 2 hours.
Few patients can take 100 gm. per day, and none can take this for
many days in succession. If the taste is objectionable, it is prob-
ably best disguised by administering in carbonated water. The
most serious objection to the oral method is the possible nausea,
and the dosage should be regulated to avoid this. Diarrhea is also
frequent. More or less edema, generally harmless, may result from large
doses. Defective or sensitive kidneys may possibly suffer injury, and
inhibition of diuresis is a possible serious consequence. On the whole,
this method is the safest and with prudence seldom results in harm.

By Rectum. — The well known drop method is the best. In deep
coma, retention and absorption are generally poor. In a less extreme
stage, this method may be the safest and most convenient substitute
or supplement for oral administration. A mixture of equal parts of
physiological saline and 4 per cent sodium bicarbonate solution (mak-
ing a 2 per cent bicarbonate) was recently given thus to a boy of 12
years for 4 days continuously, and as much as 35 gm. sodium bicar-
bonate and corresponding quantities of fluid were thus introduced
without the least difficulty or irritation. There is a possible question
whether, if the large bowel is filled with injection fluid, there may be
any effect on peristalsis higher up which will aggravate vomiting or
interfere with dosage by stomach. Otherwise there is probably no
objection to giving alkali by rectum.

Intravenously. -^Th.e usual fluid for injection is 4 per cent sodium bi-
carbonate in water or salt solution. Followers of Martin Fischer favor
hypertonic solutions, for withdrawing water from the tissues and for
promoting diuresis. Intravenous alkali injections, instead of being
among the first measures employed, should be resorted to only
reluctantly and on urgent necessity. The possible danger of the
familiar practice of injecting a liter of 4 per cent bicarbonate solution
has already been mentioned. The occasional sudden reviving effect

114 CHAPTER n

is probably due to a circulatory influence of the bicarbonate or the
fluid or both. It is ahnost always temporary, and perhaps carries
in itself the danger of later collapse. There are times when not
enough alkali can be given by stomach or rectum to prevent a danger-
ous fall in blood alkalinity. The intravenous method is then com-
monly used, but the quantities are probably most safely limited to
about 250 cc. for adults, repeated at intervals of several hours if neces-
sary. Presimiably the Woodyatt apparatus for continuous imiform
injection would be best of all. Intravenous alkali injections should be
used to keep the blood alkaU from falling too dangerously low, rather
than to try to maintain it at a normal level, but sometimes remark-
ably large quantities are required even for the former purpose. The
largest doses may be demanded especially in the severest intoxication,
which is the very time when, owing to feeble circulation, the danger
is greatest.

Since boiling changes bicarbonate into the carbonate, solutions
may be prepared in one of the following three ways: (1) by boiling the
solution, and then passing sterile CO2 gas through it to change car-
bonate back to bicarbonate, until a pink color is no longer obtained
in samples tested with phenoIphthalein;i' (2) by making the solution
without boiling, sterilizing it by filtration through porcelain; (3) by
taking clean sodium bicarbonate, preferably from a freshly opened
package of a chemically pure brand, with sterile apparatus into sterile
water or salt solution, without further sterilization." This last and
easiest method is safe enough for intravenous and perhaps even for
subcutaneous use. Solid particles are removed by filtration through
sterile cotton or filter paper if necessary. Solutions are wanned to
body temperature before injection.

Subcutaneously. — Magnus-Levy" called attention to the fact that
sodium bicarbonate, as a neutral salt without marked irritating prop-
erties, can be given subcutaneously. The method is relatively little
employed, because of the fear of infecting or damaging the susceptible
tissues of a diabetic, as well as producing pain or discomfort. One
feature of usefulness was demonstrated in the twelve year old boy

" Magnus-Levy, A., Ueber subkutane Infusionen von Mononatriumkarbonat,
Therap. Monatsh., 1913, xxvii, 838-843. Also Joslin's text, 1917, 397.

GENERAL PLAN OF TREATMENT 115

above mentioned. On his last day of life, 35 gm. sodium bicarbonate
given by rectum were only partly absorbed. 40 gm. given intraven-
ously failed to check the fall of the alkaUne reserve. The patient
was sinking into unconsciousness, with Kussmaul breathing and the
full picture of typical diabetic coma; CO2 capacity of plasma 26.5
volume per cent. A total of 90 gm. sodium bicarbonate in 4 per
cent solution was given subcutaneously between 7 :30 p.m. and mid-
night. The hyperpnea was considerably diminished; there was no
perceptible influence upon consciousness or the general condition for
either good or ill. The slow increase of intoxication continued as
before. Death occurred at 1:40 a.m., and blood taken immediately
after showed a plasma bicarbonate reading of 68.1 volume per cent.
A few authors heretofore have opposed the acid intoxication hy-
pothesis by reporting death in coma with alkaline urine. Inability
to give enough alkali has been a prevalent excuse for failure. There
is no objection to placing enough bicarbonate beneath the skin to
give the patient the benefit of any desired level of alkalinity; and
with the aid of the recent improved methods of estimating the alka-
line reserve, it is possible for any follower of the acid intoxication doc-
trine to convince himself that the patient's blood alkali can be kept
at a fully normal level, but he dies in deep coma nevertheless.

B. Infectious and Surgical Complications and Emergencies.

The methods employed in managing cases of this group are shown
in the individual histories, and the collective results are presented
in Chapter VII. The experience, though favorable on the whole, is
so limited that discussion of the treatment must be based largely on
the literature and on general principles. For the older literature,
reference may be made to text-books and the papers of Umber,i'
Kaposi,!' Kraus,^" and Karewski;^! and for developments under the
newer dietetic methods, to JosUn's text and Strouse's^^ paper. Com-

^* Umber, Deutsch. med. Woch., 1912, xxxviii, 1401-1403, 1433-1434.
" Kaposi, H., Ergebn. Chir., 1913, vi, 52-75 (128 references to literature).
^^ Kraus, F., Deutsch. med. Woch., 1914, xl, 3-8 (with statements by Naunyn,
von Noorden, and Minkowski).
^iKarewski, F., Deutsch. med. Woch., 1914, xl, 8-13.
22 Strouse, S., Med. Clin. Chicago, 1916, ii, 37-52.

116 CHAPTER n

plete discussion of surgical complications, like complete treatment of a
patient, demands the collaboration of physician and surgeon. The
present brief suggestions will omit statistics, most surgical details
and finer classifications, and will be limited to general outHnes of
practical procedure.

Certain broad dicta may be taken directly from former authors.
First, every patient coming for treatment of any medical or surgical
ailment should have the urine tested for sugar, whether diabetes is
suspected or not. There is ample proof that this admonition is far
from superfluous even today. Even with a negative test, Kaposi
urges strict inquiry for diabetes in the family or past history, and
attention to present or past obesity, suppurations, or other sus-
picious indications. Second, mildness of the diabetes and slightness
of the complication or operation promise the best outcome and the
least contraindication to surgical measures; but mild diabetes may
turn suddenly severe with a complication or shock, and a complica-
tion may be aggravated by diabetes, so that unnecessary interference
should be avoided in the presence of any active symptoms, and the
prognosis should always be guarded. The more threatening the
comphcation and the more critical the necessity of surgical inter-
vention, the less is diabetes regarded as a contraindication. Third,
the special dangers threatening the diabetic are peculiar susceptibility
to infection, subnormal healing and repairing power, and acidosis.
The last causes most deaths. The first two are largely overcome by
aseptic and operative care. Fourth, the better the dietetic prepara-
tion, the less the danger. Since acidosis is the chief peril, the best
preparation will include a maximum assimilation of carbohydrate;
therefore formerly ap oatmeal period was recommended (von Noor-
den, Addis, and others).^' Fifth, the surgical technique of an emer-
gency operation should be the simplest yet most effective possible,
avoiding shock, traumatism or long anemia of the parts, elaborate-
ness, and anything tending to lengthen the time of operation or
dispose to subsequent sloughing or infection. Sixth, local or spinal
anesthesia is considered safest from the standpoint of acidosis.
Proper general anesthesia is usually well borne by well prepared

23 Addis, T., J. Am. Med. Assn., 1915, Ixiv, 1130-1134.

GENERAL PLAN OF TREATMENT 117

patients. It should be as brief as possible. Psychic as well as
physical distress should be guarded against. The anesthetic of
choice is nitrous oxide and oxygen. Ether is more dangerous.
Chloroform should never be used for diabetics. Seventh, postopera-
tive care includes on the one hand the most skilled dieting, aiming
particularly at carbohydrate assimilation, and on the other hand sur-
gical precautions, such as exercise and other measures favoring cir-
culation and general hygiene, and avoidance of tight dressings.
Eighth, fatal coma or other disaster may occur from any sort of
operation, in any grade of diabetes, after any form of preparation,
any kind of anesthetic, and any postoperative care (Naunyn, Karew-
ski, and others). Ninth, operative relief from tumors or other
troubles sometimes has a beneficial influence upon the diabetes
(Eising and others).^ Tenth, the use of alkali stands on about the
same basis as in uncomplicated cases. The frequent occurrence of
acidosis with operation or anesthesia in non-diabetics has been brought
into some prominence of late (Crile,^^ Bradner and Reimann,*^ Bum-
ham,*' Lincoln,^' Morriss,*' and others). The recent work of Hen-
derson and Haggard^" indicates that the lowering of the carbon
dioxide capacity of the plasma does not represent a true acidosis.
Accordingly, only the acetone body production can here be regarded
as evidence of acidosis. The treatment has consisted in preliminary
carbohydrate diet, and, in emergency, glucose and sodium bicarbon-
ate, alone or separately, orally, rectally, subcutaneously, or intra-
venously. The glucose is unquestionably the more important for a
non-diabetic. The value of alkali has been questioned. Naunyn
strongly advocated saturating every diabetic with sodium bicarbon-
ate before operation, and he has had the largest following. Undoubt-
edly the blood alkahnity can be raised by alkali dosage, but there is
the open question whether artificially raising the blood alkalinity is

2* Eising, E. H., /. Am. Med. Assn., 1914, Ixii, 1244-1245.
" Crile, G. W., Ann. Surg., 1915, Ixii, 257-»-263; ^w. Med., 1916, xxii, 447^51.
2^ Bradner, M. R., and Reimann, S. P., Am. J. Med. Sc, 1915, cl, 727-733.
"Burnham, A. C, Am. Med., 1916, xxii, 438-441.

28 Lincoln, W. A., Ann. Surg., 1917, Ixv, 135-141.

29 Morriss, W. H., /. Am. Med. Assn., 1917, Ixviii, 1391-1394.

5" Henderson, Y., and Haggard, H. W., J. Biol. Chem., 1918, xxxiii, 333-371.

118 CHAPTER II

necessarily synon37inous with benefiting the patient. Alkali has not
prevented the high mortahty from postoperative acidosis in the past,
Strouse has had good results in operations with alkali, and Joslin
in operations without alkaU. The practitioner's choice in individual
cases will be governed by his attitude on the general subject.

Contrary to past practice, alcohol is at present not used in this
hospital as a food at any stage in diabetic complications or the
acidosis accompanying them.

Authors have divided complications into those for which the diabetes
is wholly or partly responsible, and those independent of the diabetes.
Therapeutic measures are sometimes influenced by theories as to the
reason why diabetics are subject to so many characteristic compli-
cations and so lacking in resistance to damage of all kinds. Notions
that excess of sugar directly injures tissues or provides a favorable
medium for bacteria have been sufficiently discredited. It is also
important to emphasize that thougli malnutrition predisposes to in-
fection, the susceptibility of diabetics is something special and
peculiar, since hunian beings or animals suffering from other condi-
tions involving equal or greater inanition and cachexia are not
afflicted in this manner or degree. As formerly pointed out," one
general conception of diabetes is apphcable also to all complications.
The present treatment is built upon the idea, supported by consid-
erable evidence in addition to the treatment, that diabetes is weak-
ness of the general nutritive function, including both cataboUsm and
anaboHsm. It is thoroughly in line with this poin^ of view that every
part of the diabetic body should manifest diminished power of main-
taining normal function, of repairing the natural wear and tear, of
healing wounds, and of resisting infectious invasions. Not only the
grosser complications, but also retinitis, cataract, arteriosclerosis,
neuritis, asthenia out of proportion to loss of flesh, and the multitude
of other disorders listed in classical text-books, accord with this con-
ception. Since the trouble is due to deficiency not of nutritive ma-
terials but of the nutritive function, relief should be expected from
strengthening this function, even at the price of dimmished food supply
and body weight. Experience indicates that this result actually

«i Men, Am. J. Med. Sc, 1917, cliii, 313-371.

GENERAL PLAN OF TREATMENT 119

follows, and that there should be no hesitation to impose rational un-
dernutrition for the purpose of raising resistance.

Complications and operations fall for practical management into
those with which there is opportunity for preparation, and those
affording no opportunity for preparation.

1. When There is Time for Preparation.

(a) Prophylaxis. — ^Just as the food tolerance is never fully restored
in typical diabetes, so also the Resistance is probably never entirely
normal. It is possible, for example, that no dietetic treatment will
ever bring the resistance to tuberculosis quite to normal, and that the
incidence of this disease will accordingly always be higher among
diabetics than among the general population. Also, if an infection
does gain lodgment, there is always the danger that diabetes will be
made worse and that resistance will collapse correspondingly. On
the other hand, resistance is probably highest when a diabetic is
kept as nearly as possible like a correspondingly undernourished
non-diabetic. Reduction of diet to something like the Chittenden
standard has never been shown to cause serious lowering of resist-
ance. Below this scale, freedom from symptoms necessitates emacia-
tion and weakness in proportion to the severity of the diabetes; but
it has repeatedly been pointed out that feeding beyond the tolerance
gives only a temporary and dearly bought benefit to weight and
strength, and it seems evident that such an attempt actually lowers
resistance at all stages. Three points of prophylactic advantage from
efficient dietetic treatment can be set down as facts. First, the long
list of complications which have been the chief torment of diabetic
patients in the past are largely prevented; a pimple does not de-
velop into a carbuncle; an abraded toe heals instead of becoming
gangrenous, etc. Second, the aggravating influence of complications
upon, diabetes is thus either avoided or reduced to a minimum.
Certain cases in the present series show the occasional possibility of
attaining the ideal that a patient shall pass through a crisis of in-
fection or operation without developing either glycosuria or acidosis;
and in a larger proportion it is possible to avert acute death and also
guard against any lasting injury to the diabetes. Third, health and

120 CHAPTER II

resistance are maintained either indefinitely or for the longest pos-
sible time, whereas overfeeding entails progressive decline in all re-
spects and corresponding liability to and damage from complications.

(&) Preparation for Emergency. — This is generally synonymous with
preparation for operation. The time available naturally varies with
the surgical condition, but something like a tumor or a quiescent
appendix may permit all necessary leisure and care. Active diabetes
is first controlled in the usual manner. A carbohydrate period is
important thereafter; and if acetone is persistent, it is probably best
to continue the highest possible carbohydrate diet without fat until
the Rothera reaction is negative if possible. The blood sugar and
all other tests should also be brought to normal if circumstances per-
mit. Meantime, protein will lower carbohydrate assimilation and
may tend to prolong acidosis, but will support strength better than
any other food. It may be called an ideal preparation which sends
a patient to operation after a fat-free diet of 1.5 gm. protein per
kilogram of weight and the highest feasible carbohydrate ration, with
all laboratory tests normal. In case of sudden damage of assimila-
tion from operation or anesthesia, this arrangement insures the
greatest possible liability to glycosuria, which is generally easy to
control, and the least possible liability to acidosis, which is the chief
danger. Joslin and Strouse give examples of preparation along these
lines. The latter, for example, prepared a woman with a fat-poor
diet of eggs and 85 gm. carbohydrate, so that the urine was free from
sugar for 15 days and from acetone for 5 days before operation. A
combined hysterectomy, right salpingectomy, and oophorectomy,
under nitrous oxide preceded by morphine and atropine, was then borne
without incident other than one day of glycosuria. While diabetes
necessarily involves operative danger, it is believed that these prin-
ciples offer the best chance of safety.

(c) Treatment with Subacute or Chronic Complications. — ^As men-
tioned elsewhere, some complications, such as nephritis, require no
departure from ordinary management. Others, such as infections
or pregnancy, have interrelations with diabetes which are important
in influencing both conditions. On the whole, the most serious
medical complication is tuberculosis, and especially the conflict is
sharp here between the overfeeding customary for one disease and the

GENERAL PLAN OF TREATMENT 121

underfeeding demanded by the other. Severe tuberculosis with
severe diabetes makes an inevitably fatal prognosis. When either
disease is mild, the chance is a little better but by no means good.
When both are mild, treatment is more hopeful. A number of
patients imder observation by recognized tuberculosis specialists
have improved strikingly when taken off the traditional high diet
and placed on a lower diet which abolished their diabetic symptoms.
It is believed that this plan, with the usual fresh air and other
measures, promises the best results with this combination.

This belief is corroborated by the experience with surgical compli-
cations, which proves plainly that tissue vitality and resistance to in-
fection are built up by treatment which controls the diabetes. The
most numerous class of surgical troubles are furunculosis and gan-
grene. The best local treatment of both is palliative and conserva-
tive. Surgical authorities seem to agree that incision of boils should
be avoided, unless absolutely demanded by spreading infection or
toxic absorption. Gangrene has been the occasion for multitudes
of needless operations and deaths in the past. Together with cata-
ract, retinitis, neuritis, and less numerous ills, it furnishes the strong-
est reason for treating diabetes in the elderly as carefully as in the
young; for notwithstanding the part attributed to arteriosclerosis or
other causes, efficient dietetic treatment prevents such troubles almost
without exception. Stetten and Lambert and Foster,'^ and others have
proved the advisability of treating gangrene conservatively when pos-
sible, with diet, measures to improve circulation, and simple local
care. Even tissues appearing dead may revive to surprising degree.
-A line of demarcation becomes established, and operation is either
avoided or reduced to a minimum. It is bad advice to operate early
and high, where the tissues and vessels are sound; and patients should
not be operated on without dietetic preparation. The only indications
for abandoning expectant treatment and operating promptly are ad-
vancing infection or fever and intoxication, not checked by other
measures and threatening danger either in themselves or in their
influence upon the diabetes. Here the treatment demanded is that

=2 Stetten, D. W., /. Am. Med. Assn., 1913, Ix, 1126-1133. Lambert, A. V.
S., and Foster, N. B., Ann. Surg., 1914, lix, 176-185.

122 CHAPTER n

for an emergency, as discussed below. Otherwise, even if operation is
later necessary, the longest possible time is afforded for preparation.
Death from amputation should then nearly always be avoidable.
The worst result recorded after such preparation is that of Baldwin,^'
whose patient's urine quickly became free from sugar and acetone,
and amputation under ether 3 weeks later was followed by death in
coma within 2 days. Owing to lack of details, it is not possible to
judge the fitness of the preparatory diet. Though such cases are
generally rather mild, yet there is always the possibility of genuinely
severe diabetes in an old person, or of continuous injury of assimila-
tion by a chronic infection, so that either early or late operation
may end in disaster. Complete laboratory tests are generally a reli-
able means of judging whether operation is safe or not.

2. When There Is Little or No Time for Preparation.

The most dangerous emergencies are the cases suddenly presenting
themselves with serious infection coupled with intense diabetic symp-
toms. Some of the examples of exaggerated nitrogen loss, maximal
D : N ratios, and uncontrollable acidosis belong in this class; e.g.,
Joslin's^* case No. 513. As the diabetes makes the infection worse
and the infection makes the diabetes worse, it is frequently impossible
to break the vicious circle, and a large proportion of such patients die.
There probably is no constant rule of diet except to exclude fat. On
the one hand, these patients are specially subject to fasting acidosis,
so that feeding with carbohydrate or protein, either or both, may be
necessary, perhaps for a majority. On the other hand, if past experi-
ence indicates correctly that ordinary coma responds better to fast-
ing than to carbohydrate, there is a chance that the same may be
true of some cases with infection, and that control of the diabetes by
the quickest and most radical means possible may be the one hope of
saving life.

As with uncomplicated cases, the plan in this hospital with infec-
tions has been to impose immediate fasting and then depend upon
clinical and laboratory indications for guidance. Chapter VII and the

'« Baldwin, J. F., Am. J. Surg., 1916, xxx, 65.

^* Joslin, E. P., Treatment of Diabetes Mellitus, 2nd edition, 1917, p. 353 fi.

GENERAL PLAN OF TREATMENT 123

case histories show the collective and individual experiences and re-
sults. Medical emergencies, even of such magnitude as lobar pneu-
monia, have for the most part been met successfully. Fasting has
benefited some patients, while others have done well on low carbo-
hydrate-protein diets. It is believed that the results on either plan
are more favorable than are possible under any method based on the
fallacy of overfeeding for the sake of strength.

Surgical complications offer one more element of hope if the sur-
gical treatment can succeed. The decision between radical and
conservative measures is often most difl&cult and doubtful. On the
one hand, dietetic control may revolutionize the surgical state and
the infection may come quickly to a standstill, when operation might
be fatal. Thus the life of the carbuncle patient No. 27 was probably
saved by immediate fasting. On the other hand, with mistaken
delay either the diabetes or the surgical condition may quickly be-
come hopeless, and what is demanded is the most prompt and radical
surgical intervention. Strouse gives an example of success due to
right judgment. A pregnant diabetic woman with threatening
acidosis was placed first on a low vegetable diet, but progressed rap-
idly toward coma. Accordingly Caesarean section was performed
under morphine and local anesthesia. Acidosis remained high for 2
days, then cleared rapidly, and the patient was soon out of danger.
The results of radically terminating a complication are apt to be
most brilliant when, as in this case, the diabetes is inherently mild
and is only stirred to intensity by the complication or by wrong diet.
Both complications and operations are extremely dangerous in severe
cases with flagrant symptoms. As the Carrel-Dakin method has
been so widely adopted by surgeons, it is only necessary to mention
the great importance of effective wound sterilization, not only for
saving gangrenous limbs, but also in carbuncles or other surgical in-
fections, to put an end to toxic absorption with the least possible
shock or delay. With advancing sepsis, a quick amputation of a
limb or removal of an appendix or other focus, even in the presence
of threatening acidosis, may save life in a minority of cases.

Postoperative care is adjusted to meet conditions. A well prepared
patient, coming through operation symptom-free, may have his diet
built up as in absence of comphcations, first with carbohydrate, then

124 CHAPTER n

with protein, finally with fat. In the presence of an emergency, the
usual choice must be made between fasting and feeding for acidosis,
following careful clinical and laboratory observations rather than any
fixed rule. Nutrition and reparative power, emphasized by Jopson,'*
are doubtless best served by protein as usual. While acidosis is the
chief danger, absence of glycosuria should be maintained or achieved
as early as possible, even at the price of lowered nutrition.

All cases of this entire group demand the constant combined watch-
fulness of the best surgeon and the best diabetic specialist available.
With this cooperation Joslin's statistics show the favorable results
obtainable in some of the most desperate cases.

5" Jopson, J. H., Tr. College Phys. Philadelphia, 1916, xxxviii, 255-257.

IV. Treatment Following Cessation of Glycosuria.

Here are to be considered (A) the carbohydrate tolerance test;
(B) the maintenance diet; (C) the period of observation and instruc-
tion; and (D) the period of after-care.

A. Carbohydrate Tolerance Test.

After a patient becomes free from glycosuria, his fast is continued at
least one day longer, so as to assure at least 24 hours of complete
sugar-freedom before giving food. This plan also is based upon the
idea of resting the weakened function. In mild cases, it is permissible
to start the test when the patient is sugar-free, even without fasting.
In severe cases with h3^erglycemia a fast-day usually precedes a
carbohydrate test, even though glycosuria is already absent. In the
severest cases of all, when the patient is extremely weak and the tol-
erance is known to be trivial, the carbohydrate period is sometimes
omitted and a period of gradually increasing protein substituted. It
may be rather important to judge the severity correctly in this re-
spect. Appearances may deceive the inexperienced, so that the
benefits of the carbohydrate period are unnecessarily sacrificed in a
patient actually possessing considerable reserve strength and toler-
ance. On the other hand, with genuinely extreme weakness there is
the possibihty of a fatal collapse of strength on the low vegetable
ration, which would be prevented by protein. This danger is really
serious only in children, because the collapse may come suddenly.
Adults weaken so gradually that there is plenty of opportunity to
avert collapse by substituting a low calory protein diet.

The standard program of the carbohydrate test has been to give
10 gm. carbohydrate the first day, and increase by 10 gm. daily until
the limit is reached. The first trace of glycosuria does not neces-
sarily represent the limit. When the first glycosuria appears, the
practice has been to repeat on the following day the same quantity
of carbohydrate which caused glycosuria. If the glycosuria disap-

125

126 CHAPTER n

pears, the regular increase of 10 gm. daily then continues, and occa-
sionally the true tolerance is found to be several times the quantity
on which the first accidental trace of glycosuria appeared. When
glycosuria occurs on two successive days with a certain intake, the
tolerance is considered to be 10 gm. less than this; i.e., the highest
quantity taken without glycosuria is regarded as the tolerance.

The test is ordinarily carried out with green vegetables, for pur-
poses of uniformity, and because they are the most bulky and there-
fore most appreciated form of carbohydrate. The benefit of salts,
vitamines, etc., in vegetables is a possible accessory advantage. On
the first days, the hungry patient is naturally best pleased with the
vegetables lowest in carbohydrate, which afford the greatest bulk.
If the tolerance is high, the bulk soon becomes excessive. As far as
possible, the patient's wishes are allowed to determine the choice of
vegetables. While the approxinaate grouping into classes of 5 per cent,
10 per cent, 15 per cent, etc., is a convenient guide in selection, it is
necessary especially in severe cases to reckon the carbohydrate of
each vegetable as accurately as possible from the standard tables, if
the test is to be at all exact. With a high tolerance, the lower class
vegetables are gradually replaced by those of higher carbohydrate
content, until finally, with the highest tolerance, bread and cereals
may be reached, though preference is given to potatoes and garden
vegetables as long as possible, in order that absorbable protein may
interfere as little as possible with the pure carbohydrate tolerance.
Fruits are also permitted during the carbohydrate test, beginning
generally with grapefruit in the earlier stages and advancing to those
richer in carbohydrate. The fruit never represents more than a
rather low fraction of the total carbohydrate intake, and with this
arrangement the fruit sugar has seemed to make no important dif-
ference as compared with starch in fixing the tolerance.

Modifications of the standard plan are used chiefly to suit var3dng
degrees of severity. It will be observed that the scheme outlined is
particularly adapted to severe cases with low tolerance. If the tol-
erance were 300 gm., an increase of 10 gm. per day would require a
month for carrying out the test. The feasibility of prolonged vege-
table diets is illustrated by cases Nos. 1 and 3, but they have no
special virtue beyond the low calories, and exaggerated length of a car-

GENERAL PLAN OF TREATMENT 127

bohydrate test is generally undesirable. For this reason the increase
in the milder cases is more than 10 gm. per day, sometimes as high
as SO gm. per day. Two points are to be borne in mind in regard to
such modifications. First, the tolerance determined by a rapid test
is by no means strictly comparable to that found in a slow test in the
same or another patient, inasmuch as the slower increase, by more
prolonged undernutrition, builds up a definitely higher assimilation.
Second, too short a test sacrifices much of the benefit, and a week or
two if possible is profitably spent as a carbohydrate period.

The purposes served by the test are diagnostic and therapeutic.
Therefore it is repeated at 6 months or other intervals, as may seem
convenient or desirable.

Diagnostic. — ^First, the carbohydrate test serves as a basis for
reckoning the subsequent carbohydrate allowance. The assimila-
tion is considerably higher for carbohydrate taken alone than in a
mixed diet, but the test gives a standard basis of reckoning. Second,
the use of a uniform test permits comparisons between patients and
between the same patient at different times, for judging both the
severity of the case and the progress under treatment.

Therapeutic. — ^First, most patients at the end of their fast have
more or less acidosis. The vegetable period, which enables the
highest possible assimilation of carbohydrate, is for this reason the
quickest and most effective means of relieving acidosis. Ketonuria
diminishes, and the. plasma bicarbonate rises without alkali dosage.
Individual peculiarities regarding acidosis may be indicated by the
varying stubbornness with which it resists carbohydrate ingestion.
Second, there is important benefit in the undernutrition, which at
first is almost like fasting.

B. The Maintenance Diet.

When the limit of tolerance has been reached in the carbohydrate
test, a single fast-day is given to clear up glycosuria. Then (or im-
mediately after the initial fast, if for any reason the carbohydrate
period is omitted) the building up of a maintenance diet is begun. A
fuU diet is not begun suddenly, for fear of bringing back symptoms.
As may be seen in the case histories, scarcely any two cases have

128 CHAPTER n

been managed identically; the regime has been individualized to suit
individual needs. With acidosis, carbohydrate is kept as liberal as
possible. For weakness, protein is raised rather rapidly to 1.5 or at
least 1 gm. per kilogram of body weight. Fat is added last, the
addition is made slowly, and the final allowance is kept within the
tolerance as nearly as this can be determined. Under the special
conditions, the fat ration is what essentially determines the body
weight, but the latter has been allowed to fall until a maintenance
diet can be assimilated without obvious diabetic s}anptoms.

A few cases in this series have been of a grade of severity indicated
by the fact that, after cessation, glycosuria would return when the
diet consisted solely of a few hundred grams of thrice cooked vegetables
on certain days or of six or less eggs on other days. With such a
trivial food tolerance, the diet is best limited to the small quantity
of protein which can be taken without glycosuria, until the assimila*
tion improves. For the most part, however, mixed diets have been
given following the carbohydrate test, the increase being preferably
limited to one class of food at a time, so as to observe the respective
effects of the addition of carbohydrate, protein, or fat. The prin-
ciples of the dietary plan were so clearly stated by Taylor'^ that
his remarks are worth quoting at some length.

"It is impossible in a discussion of so large a subject as diabetes to do more
than present briefly a few points. The clinician, even of the most advanced
modern type, who views the work that for the past ten years has been devoted
to the intermediary metabolism of diabetes ought not to obtain the notion that
this matter comprehends the substance of the disease entirely, and that upon the
elucidation of the intermediary metabolism now under investigation depends our
knowledge of the pathogenesis of the disease. Certainly, the laboratory investi-
gator has no such conception. If up to the present the laboratory investigations
have laid special stress upon the intermediary metabolism, it is because it is the
most suitable phase for investigation. Nearly aU the studies deal with abnormali-
ties in the catabolism of fat and sugar because these reactions lend themselves
to investigation. But there is a broader view-point that every laboratory man
must recognize, and which every clinician should understand, which may ex-
plain many of the divergent features of diabetes. The up-building processes of
the body can never be dissociated from the puUing-down processes. There is no
such thing as a disturbance in the burning of sugar without an effect upon the

^' Taylor, A. E., Tr. College Phys. Philadelphia, 1916, xxxviii, 254-255.

GENERAL PLAN OF TREATMENT 129

anabolism of sugar in the tissues, and likewise no disturbance in the burning of
fat without similar influence in the building-up process of fat. Fat and sugar
are vital in the building up of metabolism. We have every reason to believe that
when the body cannot burn sugar and fat it cannot utilize sugar and fat in con-
structive anabolism. Abnormalities in the utilization of sugar and fat in the
building-up processes may be as important in the production of certain symptoms
of diabetes deahng with resistance as are the abnormaUties in the catabolism.

"I would, in the second place, draw attention to one point in connection with
the current use of the Allen treatment, which is based upon a misconception.
When the diabetic has been made sugar- and acid-free, how far shall he continue
his dief ? Shall his increase of food be controlled by the urinary signs or shall he
adopt other criteria? It has not been demonstrated that it is necessary to give
the usually stated 40 calories per kilo. Investigations have recently shown that a
man of 70 kilos may live sixty days upon a diet of coarse bread, potatoes, cheese,
and eggs, containing about 2000 calories, without loss of weight. If such a man
should happen to have diabetes and were subjected to the Allen treatment, it
would be an absurdity to attempt to feed him back to 40 calories per kilo. The
man dealing with a patient should bear in mind that what he needs to feed to
is not the normally high maximum of calories but the low minimum standard of
calories."

As stated in the preliminary publications, in accordance with the
principle underl3dng the entire treatment, the fact that a person is
diabetic calls for restriction of his total diet, and, in proportion to the
severity of the diabetes as indicated by the carbohydrate tolerance,
the allowance of all three classes of foods should be diminished. With
regard, to the necessary influence of such restriction upon body
weight, it was advised that every patient, no matter how mild the
diabetes, be kept a few pounds, preferably at least 10 or 15 pounds
and in obesity more, below his usual former weight. In proportion
as the diabetes is more severe, the weight as well as the diet should
be kept lower. Overtaxing the anabolic side of metabolism by at-
tempts to make patients carry too much weight will, in accord with
Taylor's expression, bring a return of active diabetes manifested chiefly
by excretion of products of deficient catabolism; while lightening the
anabolic burden by reduction of body mass makes its benefit evident
in an unproved catabolic function.

There is a further interrelation between reduction of weight and
diet. It is known from earlier metabolic studies that undernutrition
reduces the food requirement not only absolutely but also relatively;

130 CHAPTER n

i.e., not only are there fewer kilograms of weight, but also fewer ca-
lories are needed per kilogram. A recent illustration is afforded in the
observation of Anderson and Lusk," that a dog after fasting 13 days
showed a diminution of 20 per cent in weight and of 28 per cent in
heat production. A special point in the study by Allen and DuBois
lay in establishing the influence of this principle upon diabetic me-
taboUsm. It was there shown that G. S. (patient No. 10 in the
present series), starting with a basal metabolism 2 per cent above the
average normal when severe diabetic symptoms were present, dropped
to 21 per cent below normal on the eighth day of his fast. This
calculation was based upon the DuBois height-weight formula; and
as the weight was 31 per cent below normal, the reduction below
tie original normal metabolism was far more than 21 per cent. The
reverse change was demonstrated in W. G. (patient No. 8 in the
present series). "Starting at 26 per cent below normal on January
11, when glycosuria was absent, his metabolism rose, on increased
diet and the return of active diabetes, to 20 per cent below normal on
January 15 and to 11 per cent below normal on January 22." This
patient was 42 per cent below his normal weight, so that the absolute
reduction below his original normal energy exchange was far greater.
These experiments carried out by DuBois estabHshed one essen-
tial point in this theory of treatment; viz., that a relatively high me-
tabolism accompanies active symptoms in the severely diabetic pa-
tient, and that the fasting and low diet which control these symptoms
enable him to descend to the low metabolic level proper to him as an
emaciated human being, so that his maintenance requirement falls as
low as that of any other equally emaciated individual.

Lusk"* summarized the case studied by Geyelin and DuBois as
f oUows :

"When the patient was intensely diabetic, the number of calories produced
per hour, as measured by the calorimeter, was 73.2. The weight of the patient
was 56| kilograms. The heat production was normal for that weight. Later,
through the starvation, the weight fell from S6J kilograms to 46 kilograms, and
the man developed a high degree of tolerance for carbohydrate. The calories

»' Anderson, R. J., and Lusk, G., J. Biol. Chem., 1917, xxxii, 421^45.
'^Lusk, G., Tr. College Phys. Philadelphia, 1916, xxxviii, 244-248.

GENERAL PLAN OF TREATMENT 131

produced per hour fell from 76.4 to 43, or was 35 per cent under the normal for
the lower body weight. Thus he requires only about 60 per cent of the food that
he had required previously when he was heavier and diabetic."

Patient No. 54 also was studied in the calorimeter by DuBois. The
findings quoted in her case record show that the metabolism of this
extremely emaciated woman was the lowest ever recorded, and
"only 40 per cent of the original heat production was necessary for
life."

The nitrogen output of this patient was not correspondingly re-
duced; and, though authors from Sivdn to Chittenden have demon-
strated how low the protein metabolism of normal persons may be
brought, it has been constantly borne in mind that protein is the
most essential food and its reduction the most risky of all. It must
be duly regtUated, not only because it is a food and a source of both
sugar and acetone, but also because its specific dynamic action is
greater than that of any other food in increasing metabolism. As the
body weight is low, 1.5 gm. per kilogram have been arbitrarily chosen
as a standard allowance of protein. Freedom from glycosuria is pos-
sible on a higher protein ration with fat restriction than with
unlimited fat. The new method therefore has the advantage over
former ones in this respect, and is sufficiently elastic to allow such
balance of the diet as may suit individual beliefs in favor of high or
low protein.

It is worth mentioning that the calorimetric results quoted have
been obtained with ingestion of little or no carbohydrate. Persons
acquainted with the literature need not be reminded that the in-
crease of nitrogen excretion or of total metabolism on withdrawing
carbohydrate or replacing it with fat applies only to high fat rations
or to a certain standard of metabolism; for by lowering the level of
nutrition it is always possible to reduce both total and protein metab-
olism very low, even without carbohydrate. The slightly greater
sparing power of carbohydrate is, however, one reason for retaining
it in the diet, as noted below.

Patients with the emaciation and minimal diet corresponding to the
severest diabetes are necessarily far below normal in strength. The
above mentioned investigation of Anderson and Lusk is of special
importance with regard to the muscular activity of such patients.

132 CHAPTER II

These authors proved that when a dog was reduced in weight by
fasting, there was a saving of energy when the animal ran in a tread-
mill, because less energy was required to move the lighter body. But
when the calculation was based upon the absolute work performed,
the expenditure of energy was exactly the same before and after
fasting; that is, the organism can economize in its basal metabolism,
but the same absolute labor costs the same absolute energy, irre-
spective of the state of nutrition. In diabetes, however, there are
additional factors, namely the non-utilization of much of the energy
contained in high diets, and the preternatural weakness and lassitude
due to the resulting intoxication. Williams'^ has carried out a unique
investigation by dynamometer tests of patients under treatment,
demonstrating directly an increase of muscular strength when the diet
is reduced so as to bring it within the metabolic capacity.

The following are fair conclusions from the evidence at hand. Per-
sons with mUd diabetes are as a rule easily enabled to maintain them-
selves on mixed diets with moderate restrictions which reduce their
weight but raise their efl&ciency and comfort practically to normal.
Persons with moderate diabetes require more rigid restrictions,
which bring them more or less below normal, but yet their diet is more
agreeable and their comfort and usefulness maintained both higher
and longer than on limitation of carbohydrate alone. Patients with
severe diabetes necessarily face the hardest conditions. The investi-
gations have shown the enormous load of useless and injurious metab-
olism carried by such patients with their active symptoms, and the
striking reduction of this burden under treatment which controls
symptoms. The low metabolism and efficiency of inanition remain.
There may be a tendency to calculate diets which appear absolutely
low, but yet are luxus rations for this state and injure assimilation
accordingly. The sympathy of the inexperienced onlooker is strangely
greater for weakness and emaciation held in check by a tight rein on
diet, than for the worse and rapidly progressive condition which, on
overfeeding, appears as the simple consequence of the disease. It is
possible for any case under unskillful restrictions, and for a few cases
even under the most expert care, to end in actual death from starva-

'8 Williams, J. R., Arch. Int. Med., 1917, xx, 399-408.

GENEILA.L PLAN OF TREATMENT 133

tion; but Joslin's and the present statistics agree in showing that this
is not one-tenth as frequent as other causes of death, notably coma.
Had circumstances permitted, the present series of cases might have
afforded unusual material for a study of undernutrition, and might
also have established the lower limits of a maintenance diet, which at
present are unknown. It can only be said empirically that with re-
markably few exceptions the curve of falling weight and the curve of
rising assimilation meet at a level on which life can be maintained.
The best experience seems to agree that, when such treatment is
properly carried out, the unavoidable hunger and disabiHty are less
distressing to all concerned than the troubles accompanying acidosis
and complications under former methods.

C. The Period of Observation and Instruction.

Treatment can seldom be inaugurated or patients instructed as
satisfactorily elsewhere as in a hospital with a well conducted metab-
olism ward. This statement apphes not only to the critical cases,
where the advantages are most evident, but even to the mildest ones.

For the physician, a hospital offers the best facilities for the two
prime essentials of treatment, accurate diet and laboratory control.
He is also spared much unnecessary labor and inconvenience if the
organization is right.

For the patient, a hospital offers relief from work and worries, and
both theoretical and practical education concerning diabetes. One
test of treament is found in the fact that under proper conditions a
patient is benefited by contact with other patients. Any fears con-
cerning his own initiation are relieved on acquaintance with others
who have gone through the same or more. He sees and hears the
actual consequences of following or breaking diet, and his choice is
generally for fidelity. He falls naturally, into the habits of his en-
vironment, and learns so much from his neighbors and the general
atmosphere of the place that instruction is made very easy.

Much of the benefit of the early stage of treatment is often lost by
undue brevity of the observation period. The extremely long hos-
pital sojourn of most patients in the present series is accounted for
partly by the severity of the cases, and partly by the requirements of

134 CHAPTER II

investigation. Few patients can remain in private institutions so
long, but also comparatively few cases are so severe. It may seem
that little is really being done after the first brief period of most active
treatment, and that a longer stay imposes a cost in time and money
which is unjustifiable, especially for poorer patients. It is unfortu-
nate that poverty and necessity shorten the hospital period in-
juriously in so many cases, and that public institutions are gener-
ally so ill equipped to care properly for diabetics. Also much is ac-
complished by the classes, clinics, and social service work conducted
for diabetics by some of the best institutions and specialists. But, as
a rule, the ideal hospital experience for a mildly diabetic patient can
seldom be less than 2 weeks, and for severe cases the time may extend
into months.

For observation, this period is useful in order to determine the true
food tolerance, so as to plan a diet which is neither too high, thus
causing injury of assimilation and later relapse, nor too low, thus
occasioning unnecessary privation and loss of weight. Laboratory
tests, employed as described hereafter, are the chief means of judging
progress. The patient should not be discharged until these tests give
either normal results or adequate assurance of continued progress in
the right direction.

For instruction, this period is used to equip the patient with a
sufiicient working knowledge of the care of his own case. Experience
has shown that the simple essentials can readily be mastered by even
the least educated persons, if they are willing and conscientious.
Diets are readily calculated by the more intelligent patients, especially
as the plan followed is so simple. Uneducated patients are sent out
with fixed written menus, together with a list of absolute quantities
of other foods which may be substituted for individual dishes on the
standard menu. Before leaving, a patient generally spends most of
his time for about a week in the diet kitchen, participating in
the actual preparation of his own and others' diets. He is thus
of some service, and at the same time acquires practice in cook-
ing and calculation which guards against mistakes at home. .
Men, women, and children alike are generally put through this prac-
tical training; but when a relative, servant, or other individual will be
largely concerned in the actual labor, this person is also given the

GENERAL PLAN OF TREATMENT 135

course of instruction. For testing the urine, the Benedict sugar
method alone is sufficient, and can be learned by anybody. The
tests, in severe cases or if the blood sugar is high, are best carried
out upon the four separate urine specimens of each 24 hours, as done
in the hospital. There is no harm in patients' learning as many lab-
oratory reactions as they like, but the sugar test is really all they
need to know, and they are more liable to become morbid over too
many tests. Under proper conditions, only very rare patients are
made nervous or hypochondriacal by performing their own sugar
tests, so that these must be made for them by other persons. They
must be equipped with definite knowledge of what to do if glycosuria
appears. The best psychic state is generally assured when they
know they are regularly and consistently sugar-free, and have confi-
dence in their ability to control glycosuria if it appears.

D. The Aeter-Care.

The period of after-care properly extends over the remainder of the
patient's life. For a considerable time at least, he should keep an
accurate record of the facts pertaining to his case, most conveniently
on a printed form supplied for the purpose. Such a record should
include the naked weight, the exact diet, the urinary reactions, and
the subjective health. No matter how thorough the instruction in
hospital, questions and difficulties often arise, especially in the early
period after returning home. The patient is encouraged to ask
advice when needed, but particularly is ordered to report regularly at
intervals ranging from one week in severe cases to several months in
mild cases. Some reports may be made by letter, especially by pa-
tients at a distance, but it is necessary for intelUgent supervision"
that the patient present himself in person at definite times. Occa-
sional emergencies also arise, and the patient should have some
knowledge of how to meet them. For example, many may profit
by the advice that in case of any infection, they should immediately
omit fat from the diet. But such an emergency should be reported
without delay to the physician in charge, in order that he may superin-
tend any further measures necessary.

136 CHAPTER II

When a patient reports in person, his naked weight and a urine and
a blood sample are taken. The accuracy of his record is thus checked.
If the blood sugar is normal, and the nitroprusside test is negative in
urine (Rothera) and in blood plasma (Wishart), practically nothing
else is needed. If all is not so favorable, such other analyses are
performed as may be necessary to show whether there is danger or
what is the direction of progress.

These occasional tests are the guide for such adjustments of diet
as may be necessary from time to time. The severely diabetic
patient requires rather close supervision for checking wrong tenden-
cies in their incipiency and for the best results in general. The en-
couragement and moral support gained in personal contact are fur-
thermore specially important in the severe cases, though a high pro-
portion of milder cases without it will sooner or later go wrong. A
case lost from sight is generally a failure. Milder diabetes should not
involve invalidism or irksome dependence; but these persons, even
while leading comfortable and useful lives, should keep in touch with
their medical adviser, for experienced oversight of their condition and
diet and for information concerning advances in treatment.

V. Ideals of Diet and Laboratory Control.

In the earliest preliminary outlines of this treatment, the plan was
defined as an attempt to spare a weakened function by rest, and to
this end it was proposed to make and keep every patient free from
glycosuria and from obvious acidosis. This initial step appeared as a
sufi&ciently radical, even hazardous, departure from the former man-
agement of severe cases; and it was hoped that there might be more or
less improvement in such assimilative function as remained to these
patients, corresponding to the gain in tolerance known to occur when
the symptoms of milder diabetes were cleared up under the old treat-
ment. The reality of such improvement in many of the most intense
cases in their earlier stages is now a familiar fact, and is discussed in
Chapter VII. Even in the first patient, however, the inability to
gain in assimilation to any important degree was manifest, and other
cases quickly confirmed the fact that prolonged severe diabetes was
characterized under this plan by permanently low food tolerance,
and that downward progress was merely delayed and not prevented.
The obvious path for investigation was to determine whether the
degree of functional rest represented by the crude tests originally se-
lected is adequate for such extremely severe cases of diabetes as
were intentionally selected for trial of the treatment; and this also
would have answered the question whether or to what extent there
is a genuinely spontaneous downward progress in diabetes of any
type. At this earliest period, the question was discussed with
Joslin whether it might not logically be required to abolish hypergly-
cemia rather than merely glycosuria, and whether it is possible to
bring the blood sugar to normal in the severest cases. Under the con-
ception of diabetes as a weakness of the total metabolism, it would
have been necessary to carry out simultaneous studies of the carbo-
hydrate, protein, and fat functions; to determine whether overstrain
of any side of metabolism was present; whether such overstrain was
demonstrably injurious; and whether the overstrain and injury could
be obviated. Such' studies upon a few cases would have given an

137

138 CHAPTER n

early answer to the essential question. In the first patients, it was
not possible to perform even blood sugar analyses. With the expan-
sion of laboratory facilities, the therapeutic problem became replaced
by others; and in consequence, treatment was applied to a long
series of patients over a long period of time with no advance over the
original crude criteria. That is, negative sugar and ferric chloride
reactions in the urine were maintained if possible, as originally rec-
ommended; but hyperglycemia, ketonemia, and the excretion of sev-
eral grams of acetone bodies with increased urinary ammonia daily,
as shown in the records, were allowed to continue without investiga-
tion of their possible consequences or the development of any further
means to combat them.

This poKcy has been followed by disastrous results, both in the
present series, and in the experience of others with the same method.
Meanwhile, experiments upon partially depancreatized dogs have
shown similar conditions. After suitable operation, a dog on a given
diet may be free from glycosuria and yet have hyperglycemia. One
of two things happens. Either the hyperglycemia passes off and the
animal lives indefinitely, or hyperglycemia persists, with or without
ketonuria, and the progressive decline duplicates that of corresponding
human diabetics. This outcome in animals which are demonstrably
free from spontaneous downward tendency furnishes decisive proof
that this degree of functional overstrain may of itself produce this
result.

This fact does not conflict with the observation of Mosenthal,
Clausen, and Hiller^" concerning the stubbornness of the tendency to-
hyperglycemia in severe diabetes. For practical reasons, it may some-
times be necessary to allow patients to go along with this level of
blood sugar which assists their defective power of combustion, appar-
ently by mass action. It is surprising how well many patients can.
do under such conditions, and for how long a time. But the down-
ward progress which ultimately follows this overstrain cannot prop-
erly be called spontaneous. Also, the greater the genuine severity
of the case, the more quickly and obviously does this continuous,
hyperglycemia bring disaster. It is belifeved that the utmost effort

^0 Mosenthal, H. O., Clausen, S. W., and Hiller, A., Arch. Int. Med., 1918,
xxi. 93-108.

GENERAL PLAN OF TREATMENT 139

should be made to maintain normal blood sugar at any stage; but
above all, proper treatment demands that a case be so managed from
the earliest diagnosis that the tendency to hyperglycemia shall be
prevented or delayed as long as possible.

The conditions described above do not apply to dogs with pancre-
atic atrophy or to occasional human patients with organic disease
obviously progressive in character and causing decline irrespective of
diet. Time has not yet permitted answering the other half of the
question; viz., whether the great mass of typical diabetic patients are
ultimately subject to downward progress even when all functional
overstrain is relieved as far as ascertainable.

As shown in Chapter VII, results have been decidedly best when
early cases of diabetes have been so treated as to keep them normal
to all the chemical tests used. In resuming the therapeutic prob-
lem recently, difficulty was anticipated in a large proportion of more
advanced cases, because the hyperglycemia is often very refractory
to fasting. It has proved possible, however, to achieve a normal
blood sugar in almost all cases on a plan prompted by the following
reasoning.

Reduction of body mass has been a regular means of improving
assimilation. But if it were desired only to relieve of his obesity
one of the fat patients in the series, the best method would be neither
plain fasting nor a haphazard mixed diet. The rational diet for
obesity is one containing protein to protect body nitrogen and bulky
vegetables to fill the stomach, while low in calories so as to compel com-
bustion of body fat. An obese person can endure such a treatment,
when on plain fasting he might become dangerously weakened before
his weight was sufficiently reduced. The same considerations apply
with greater force to weakened diabetics. By subjecting these
emaciated patients to an obesity cure, their weight has been reduced
sufficiently to conquer their hyperglycemia. This means, in practical
application, that after the initial fast and carbohydrate test, if the
blood sugar is still high, the patient receives a diet in which the only
real food is protein, generally about 1 gm. per kilogram of body
weight. Body nitrogen is spared and strength maintained better
than on plain fasting, and the program is continued until the blood
sugar falls to 0.1 per cent. The specimen laboratory chart facing

140 CHAPTER n

page ISO illustrates such a treatment, through the periods of the
initial fast, the carbohydrate test, then the protein diet till the blood
findings are normal, and fina,lly the mixed maintenance diet. Rare
cases are so severe that both hyperglycemia and ketonuria persist
for weeks on this exclusive protein diet. Here it has been necessary to
keep the patient for a week or two on a diet with negligible food values,
viz. soup, bran, agar jelly, and thrice cooked vegetables, in order to
obtain normal blood sugar, which may then contmue on the above
protein diet. Protein is increased if possible to 1.5 gm. per kilogram
of weight. The first food added to it is carbohydrate, and a patient,
according to severity, is required to assimilate 5 to 20 gm. without
hyperglycemia, and thus to be free from any trace of ketonuria, be-
fore proceeding to the gradual addition of fat. The limit of fat and
calories in the maintenance diet is governed by laboratory tests.
The importance and interpretation of these tests change in the later
observation period from what they were at the inception of treat-
ment, and a few remarks may be devoted to the three phases of
metabolism involved.

Protein. — No direct tests of protein metabolism are required in the
late observation period. Most important would be total nitrogen
analyses in any case of doubt concerning the nitrogen balance, but
on the protein allowance recommended the patient ordinarily comes
into nitrogen equilibrium with simple clinical observation. Am-
monia is always normal if acidosis is controlled as described. Un-
published analyses in this laboratory have shown that in the most
intense active diabetes there is increase of amino-acids both in the
urine, as reported in the literature, and in the blood; but this, like the
exaggerated nitrogen catabolism, is regularly absent under the
routine treatment. Sufficient warning of an overtaxed protein me-
tabolism is afforded by hyperglycemia or ketonuria.

Carbohydrate.— With. Benedict's method,*^ it is now as easy to de-
termine the sugar in blood as formerly the sugar in urine, and really
simpler and more satisfactory to make the analysis than to send the
blood to a laboratory. One hindrance to its use by practitioners has

" Lewis, R. C, and Benedict, S. R., /. Biol. Chem., 1915, xx, 61-72. Benedict,
S. R., ibid., 1918, xxxiv, 203-207. Bock, J. C, and Benedict, S. R., ibid., 1918,
XXXV, 227-230.

GENERAL PLAN OF TREATMENT 141

been the cost of a colorimeter, which has been met by the introduction
of the Bock and Benedict^' instrument. Epstein' s*^ modification of
the Benedict method, though not quite so accurate, is the sim-
plest and cheapest of all and requires only a few drops of blood, ob-
tainable from the ear or finger. A large number of physicians whose
tests must be made in their own offices and who would never under-
take a more elaborate method, will undoubtedly make use of this
device, and will have no excuse for being without blood sugar analyses.
Knowledge spreads rapidly among diabetic patients, and instead of
objecting to the drawing of blood many of them doubtless will soon
be demanding it.

If the blood sugar is kept normal, urine tests are almost superfluous.
The patient has the agreeable knowledge that glycosuria is always
absent, and his tests merely guard against errors in diet or any un-
foreseen change. The blood sugar is one of the most delicate indi-
cators not only of the carbohydrate but of the total metabolism.
Even though glycosuria be absent, a dangerous lack of control of the
diabetes is indicated in those instances where the blood sugar actu-
ally rises after one or several days of fasting. It is sometimes but not
necessarily associated with a correspondingly unfavorable change in
the acidosis. The h3^erglycemia after carbohydrate ingestion rises
and falls relatively quickly. There is a more gradual rise and fall
after protein. The absence of hyperglycemia after feeding pure fat,
and the slowness of the rise of blood sugar on adding fat to a diet,
are in accord with the accepted belief that fat is not converted directly
into sugar; but the h3^erglycemia is particulatly lasting and stubborn.
The limit of fat in a maintenance diet is reached when hj^erglycemia
results from its further addition to the ration of protein and carbo-
hydrate which has been fixed as necessary. The ideal is that the
blood sugar shall not be above 0.1 per cent fasting or above 0.15 per
cent during digestion.^

*^ Epstein, A. A., /. Am. Med. Assn., 1914, Ixiii, 1667-1668. Instrament with
instructions obtainable from Ernst Leitz, 30 East 18 Street, New York City.

■*'As this monograph goes to press, the first of a sferies of papers from the
laboratory of S. R. Benedict, who has already contributed so preeminently in the
field, are appearing in The Journal of Biological Chemistry, 1918, xxxiv, 195-262.
The application of a newly perfected method, which determines quantitatively

142 CHAPTER n

Fat. — The two direct evidences of disordered fat metabolism are
acidosis and lipemia, which will be considered separately.

Acidosis. — Quantitative tests are necessary precautions when
acidosis exists; but as far as now known, there is no danger from
diabetic acidosis if the nitroprusside test is negative in both urine
and blood plasma." It has proved possible to keep the reaction con-
sistently negative in some of the severest cases of diabetes. A ques-
tion is possible whether strictness to this degree is necessary: whether

the sugar even in normal urine, gives promise of results of the highest importance
in the study of sugar tolerance and carbohydrate metabolism. The prediction
may be ventured that such a refined method will reveal a pathological excretion
of urinary sugar by diabetics with the familiar marked hyperglycemia. In-
vestigation will have to show whether the urine becomes normal for sugar when
the above requirements of normal blood sugar are fulfilled. It is to be empha-
sized that the essential progress and improvement of clinical results must lie in
this direction of finer methods, earlier diagnosis, and stricter control of incipient
abnormalities. Only by such means can the principle of treatment by sparing
a weakened function be carried out successfully.

** Legal (Z. and. Chem., 1883, xxii, 464) first observed that the nitroprusside
reaction (originated by Weyl as a creatinine test) might serve as a test for acetone
and acetoacetic acid. V. Arnold {Centr. inn. Med., 1900, xxi, 417), by fine
quahtative tests showed that acetone is excreted only in the severest grades of
acidosis, while the substance present in ordinary so called acetonuria is aceto-
acetic acid. Embden and Schliep {Centr. ges. Physiol, u. Path. Stqffwecks.,
1907, ii, 289) found quantitatively no preformed acetone in the fresh urine in
some cases of ketonuria, and in other cases it ranged about 1/10 to 1/4 of the total
acetone bodies. Folin and Denis (/. Biol. Chem., 1914, xviii, 267) stated that
"acetone urines contain from two or three to nine or ten times as much aceto-
acetic acid as acetone." Rothera (/. Physiol., 1908, xxxvii, 491) regarded his
improvement of the nitroprusside test as a test for acetone; but W. H. Hurtley
{Lancet, 1913 (1), 1160) proved that with pure materials the Rothera reaction is
sensitive to acetoacetic acid in 1 to 400,000 dilution, but to acetone only in 1 to
20,000 solution. Kennaway {Guy's Hasp. Rep., 1913, Ixvii, 161) confirmed the
fact that the Rothera test is essentially an acetoacetic test which is at least 25
times as deUcate as the Gerhardt ferric chloride reaction; and he suggested that
the greater opportunity and ease of diffusion through the lungs as compared
with the kidneys is the reason why most of the preformed acetone leaves the
body through the former. There is no simple qualitative test for /3-oxybutyric
acid. To some extent the intensity of the acetoacetic reactions serves as a rough
index of the quantity of both acids present, but there are wide departures from
this rule in both directions.

GENERAL PLAN OF TREATMENT 143

normal persons with identical nutrition would not show slight keto-
nuria, and whether it may not be harmless. There is an opposite
speculation whether a diet or metabolic state productive of keto-
nuria is not more or less harmful even to normal persons, and whether
a diabetic may not be more susceptible to injury. The presence of
|3-oxybutyric acid out of proportion to the small acetone-acetoacetic
"fraction seems to characterize some of the long standing severe cases.
Any considerable ketonuria in severe cases is associated sooner or later
-with hyperglycemia. When the blood sugar is low, faint nitroprusside
reactions have been allowed to exist in some patients, without empiric
evidence of harm. While ketonuria is most closely associated with the
fat ration, it can result directly or indirectly from unwise addition of
•any kind of food to the diet. When acidosis in the strictest clinical
•definition is kept absent as described, the plasma bicarbonate is regu-
larly high, generally above rather than below 65 per cent.

Lipemia. — ^The investigation of this subject is apparently of rapidly
;growing importance. It has long been known that some cases of dia-
betes are characterized by lipemia far in excess of anything found in
any other condition. Some of the facts recently established^ are
that the blood fat may be several times the normal without notice-
able turbidity; that the lipoid relations, especially the high cholesterol,
-are in contrast to normal alimentary Hpemia; that in severe diabetes
the hyperlipemia is apparently as constant and characteristic as the
Tiyperglycemia, and that it is largely associated with the fat intake
and with other active diabetic sjonptoms. At present, the findings
•seem to support the conception of diabetes as a disorder of the
total metabolism, and to furnish further evidence against the mis-
leading practice of labelling phloridzin, adrenalin, or other forms of
-sugar excretion as "diabetes." The question immediately arises
whether excess of fat in the blood is not as truly indicative of over-
^strain and injury as excess of sugar. It is also essential to know
whether the rigid program above outUned brings the lipoids as well as
other blood constituents to normal. The work of Gray^^ shows actu-
.ally low levels of blood fat in some severe cases under strict treat-
ment. Many analyses are also under way in this hospital. It is

"Allen, Am. J. Med. Sc, 1917, cb'ii, 313-371. Gray, Boston Med. and Surg.
J., 1918, clxxviii (references to Bloor and Joslin).

144 CHAPTER II

not yet certain whether fat determinations are necessary for guid-
ing treatment at this stage. The blood sugar and nitroprusside tests
may perhaps suffice.

It should be emphasized that comparison and clinical judgment are
necessary in interpreting the significance of all laboratory tests. It is
wholly erroneous to consider that hyperglycemia, ketonuria, or any
other laboratory finding is in itself proof of a breaking strain upon
metabolism, or that absence of such indications gives assurance that
all is well. As in dogs, so in patients, hyperglycemia may gradually
subside on right diet or may gradually develop on wrong diet. The
same is true of ketonuria, and doubtless also of lipemia. Some pa-
tients in this series have been discharged with marked hyperglycemia
and ferric chloride reactions present. These persisted for months,
but yet the policy was safe, because it was recognized clinically that
the cases were essentially mild diabetes, and that these symptoms
would gradually clear up, without requiring that an elderly or weak
person be subjected to more serious privations. Such liberties with
a severe case, even though tlie remaining symptoms be slight, are
risky; and they are disastrous with any case unless the diet is within
the actual tolerance. It is highly important not to treat an incipient
case of potentially great severity as if it were a genuinely mild case.
Also, in some severe cases in this series, the blood sugar was sometimes
brought to normal by withdrawal of carbohydrate, with a diet too
high in fat and calories. More or less ketonuria was present, and
doubtless the blood fat was high. Notwithstanding absence of hyper-
glycemia for weeks or months on carbohydrate-poor diet, such a case
can be expected to go steadily downhill. The character of the case,
comparisons of different tests, and the direction of progress are there-
fore important guides in treatment and prognosis. Too much em-
phasis upon any single test may be as misleading as the lack of tests;
and though laboratory work should never be slighted, the experienced
man with very simple means will administer far better and safer
treatment than the tyro with a great laboratory at his disposal.
The ideal treatment therefore begins with rather extensive laboratory
study, but in the end comes down to a very few simple tests.

While discussing ideals, the fact should be plainly faced that the
program above suggested is for very severe cases an excessively rig-

GENERAL PLAN OF TREATMENT 145

orous one. The patients of this extreme type are weakened by it;
sometimes they must be temporarily kept in bed; and their physical
and psychic depression becomes greatest at about the time the blood
sugar becomes normal. No disaster has occurred under the method,
and none of these patients has refused it. Strength returns when a
maintenance diet is resimied; sometimes it seems as great as before,
but more often the fall in both flesh and strength is noticeable. In
view of the questionable prognosis in such extreme cases at best,
the conservative physician will ask himself whether it is advisable to
impose such privation, especially as inanition and the dangers of
chance infections are obviously brought closer. In a few cases, mod-
erate hyperglycemia and shght nitroprusside reactions without other
symptoms have been permitted in the interests of strength and
efficiency. Similar ideals have suggested themselves to a number of
the best workers in this subject, on account of their similar mishaps
with the less careful methods. As far as known, however, both the
plan and execution of the above program are new. It has been appHed
because the patients wished to live, and because it was certain that
they would die soon unless saved by radical measures. Their sub-
jective comfort after the rigid treatment has been about the same as
before. The downward progress formerly evident has in every in-
stance been either arrested or delayed — the few months of experience
do not permit answering which. It is not certain whether such a
method is to be generally recommended in practice, and in any event
there is no desire to urge it upon either physicians or patients. It is
fairly certain that the rigid plan will prolong life and also maintain
a fixed level of nutrition, if not indefinitely, at least considerably
longer than laxer methods. If hyperglycemia, ketonuria, and other
symptoms are allowed to persist, a definitely gloomy prognosis must
be accepted, and the choice is essentially either death in coma or pro-
gressively more severe undernutrition, which becomes more extreme
than required under the rigid plan and increases to death in starva-
tion. The above quaUfications apply, however, only to these cachetic
patients with excessively severe diabetes. The greatest importance
of the plan lies in its application to earlier cases, and for these it is
strongly and unreservedly recommended. In the early stage it is
shorter and easier to carry out, involves no extreme privation or

146 CHAPTER II

physical deterioration, and fulfills the purpose of relieving metabolic
strain as far as present analytic methods can determine. It has
thus far demonstrably prevented downward progress in several cases
of the type which ordinarily progress downward, and it offers at least
a chance of continued subjective health, whereas looser methods prom^
ise nothing but death.

When the blood sugar is normal, glycosuria from trivial carbohy-
drate ingestion does not occur. Accurate reckoning of the diet is
just as essential; but yet if glycosuria results from slight fluctua-
tions in the carbohydrate content of vegetables, or from adding a few
hundred grams of thrice cooked vegetables, the patient is certainly
too close to the verge of his tolerance and trouble will follow unless
the condition is improved. There are the following reasons for giv-
ing carbohydrate as prominent a place in the diet as feasible. First,
it gives the quickest and most harmless danger signal. Second, at
least a small quantity is necessary to fulfill the ideal of freedom from
ketonuria. Third, it spares protein more effectively than fat, and
incidentally spares the total metabolism somewhat; and as shown by
Zeller,*^ if the carbohydrate of the ration is equivalent to one-tenth
of the fat calories, the sparing is as effective as though all the fat were
replaced by carbohydrate. Fourth, by permitting a supply of fresh
green vegetables, it makes a diet more agreeable and satisf3dng than a
higher carbohydrate-free ration. Fifth, on general principles and for
reasons partly unknown, a mixed diet is the only natural diet, and
no diabetic will ever live long on any other. Caution is needed
against the mistake conamitted by some, in giving so much carbo-
hydrate that a living ration of protein and fat is made impossible.
But as stated, the rule in this hospital recently has been to reduce
the total diet sufficiently to enable any patient to assimilate at least
5 gm. of carbohydrate, and correspondingly more in the less extreme
cases.

Various methods of treatment have been tried in the present
series. At one extreme there has been reversion to the old practice
of carbohydrate-poor diets of 40 calories per kilogram or more.
At the other extreme are a few cases treated according to the rigid

^"ZeUer, H., Arch. Physiol., 1914, 213-236.

GENERAL PLAN OF TREATMENT 147

program last outlined. The results shown are therefore not those of
any one method. The results of different methods should be compared
and the choice of treatment governed accordingly. The experience
is believed to support the original principle that treatment should
aim to spare a weakened total metabolism, and that in proportion as
carbohydrate must be restricted, the total diet should also be kept
low.

VI. Practical Management of Diets.
A. Organization.

Many physicians and hospitals have found it possible to conduct
diabetic treatment more or less successfully under adverse conditions.
Foods may by special arrangements be served from the general kit-
chen if necessary. Though some patients in the present series, es-
pecially in observations requiring accuracy, have been isolated in
individual rooms, others have been in open wards with patients suf-
fering from other diseases. Their own fidelity, and the knowledge
that glycosuria and fasting would follow an indiscretion, have main-
tained a high general average of good conduct.

The ideal arrangement, and the one which is being rapidly adopted
by the best hospitals, is to organize a special diabetic or metabolic
ward, with a separate diet kitchen in as convenient proximity to it
as possible. The kitchen organization here, and the cooperation of
Miss Emmeline Cleeland, the diet nurse, have contributed much to
the success of the work.

The head of the kitchen may be either a specially quahfied nurse
or a trained dietetian who is not a nurse. Her time is best left
free for duties of supervision. The physician has merely to order a
diet in terms of protein, carbohydrate, and calories. The nurse then
translates these figures into the actual foodstuffs, superintends the
cooking, and is responsible for the accurate recording of everything
pertaining to the diet. She maintains a sympathetic acquaintance
with all patients, takes care that the selection and preparation of food
suits their tastes as well as possible, and by smoothing small diffi-
culties contributes greatly to lighten the lot of the patient and the
labor of the physician. Under some circumstances it may be con-
venient for one nurse to have charge of both the kitchen and the
ward, and to supervise also the qualitative testing and recording of
the urine.

The assistant diet nurses vary in number with the number of
patients and the degree of detail required. Labor is saved at the

148

GENERAL PLAN OF TREATMENT 149

expense of some slight inaccuracy by weighing certain foods after
cooking, by estimating certain other foods, etc. Servants at lower
wages can save both the nurses' time and some of the more dis-
agreeable features of the work. In this hospital every kind of food
has been weighed accurately raw, and cooked separately for each
patient. With this arrangement, one assistant nurse for about eight
patients has been needed. If the service is rotating, an assistant
nurse should if possible spend at least three months in the kitchen con-
tinuously; otherwise both time and accuracy are sacrificed in teaching
new nurses. At the end of the three months she should be familiar
not only with the cooking but also with the duties of the head nurse.

B. Equipment.

The equipment is mostly that of an ordinary kitchen. A few
special articles have been found useful, as follows:

Diet scales. — An accurate spring balance has been used for weighing
the individual food portions. In construction it is similar to the or-
dinary letter scales. This model is manufactured* by Chatillon and
Company, 85 Cliff Street, New York. The price, formerly $5.00, is
now $7.50. Each patient buys such a balance preparatory to return-
ing home. The dial is movable, so that it can be set at zero after
the dish for receiving food is placed on the weighing stage. The
weight of the food can then be read directly in grams. The quickness
and convenience of such an instrument is important for prolonged
fidelity in weighing food, for few patients will trouble themselves
through months and years with the tediousness of ordinary scales
and weights.

Steamer. — A well known form of steam cooker has been used for
cookirig vegetables without loss of carbohydrate. The reservoir at
the bottom contains water; the compartments above hold the vege-
tables. As the steamer is constructed on the unit system, few or
many of the compartments may be used at any time as needed. By
this means a number of different vegetables can be steamed simul-
taneously, and the more easily cooked ones can be removed before
the others.

Slide Rule. — Nurses who are to calculate many diets can save time

150 CHAPTER n

and trouble in multiplication by learning to use a simple slide rule.
A convenient one is the "Merchant's," obtainable from the Keuffel
and Esser Company, 127 Fulton Street, New York City.

Adding Machine. — ^Additions have been performed with the Golden
Gem Adding Machine, manufactured by the Automatic Adding
Machine Company, 148 Duane Street, New York City. A small and
inexpensive instrument of this sort aids not only in time-saving but
also in accuracy.

Records. — ^A twofold record of diets has been kept. A more de-
tailed separate diet chart shows each individual food item for each
meal, together with the totals, as illustrated in the specimen diets
hereafter. A statement of the totals for the day is also entered in
the laboratory chart, in order that the relation between diet and
laboratory findings may be evident at a glance.

One general form of laboratory chart has been used since the early
organization of the work, with slight modifications as needed from
time to time (Table III). It measures 30 by 90 cm., and folds so as
to conform to the clinical charts. In the table two figures are given
for carbohydrate, protein, and fat for each day. The upper figure (in
bold face type) denotes calories, the lower figure (in ordinary type)
grams. For convenience in entering on the chart, the two figures
are written in the form of a fraction; the figure above the line
(calories) is written in red ink, that below the line (grams) is
written in black ink. Formerly there was a column for alcohol,
but this has been dropped, and if alcohol is given on any rare occasion,
it is written into the total calory column. There also was formerly a
column for sodium bicarbonate, but as this is so seldom used, the
column has been discontinued and any occasional doses of alkali en-
tered in the "Remarks" colimin. Among foods, three colimms are
found under "Bacon," the abbreviations indicating the three forms
in which it is served; first whole bacon; second crisp bacon, fried so
as to reduce the fat content as low as possible; third the clear bacon
fat, practically free from protein. These three forms serve different
purposes, and yet the advantage of the bacon flavor is retained. The
two columns under vegetables show the total weight respectively of
carbohydrate-containing or thrice cooked kinds. The various "Re-
marks" columns give room for additional analyses or special notes,
explanations, time of day, etc.

GENERAL PLAN OF TREATMENT 151

C. Notes on Special Features of the Maintenance Diet.

1. Fast-Days. — Occasional single days of fasting or greatly reduced
diet have been prescribed in the after-treatment of all cases. They
are taken at regular fixed periods, the length of the interval and the
rigor of the program being proportioned to the severity of the diabetes.
In the typical severe cases, a fast-day is taken once each week, the
patients generally choosing Sunday for the purpose. In even the
mildest cases, such a day is ordered at least once a month, more
commonly once every 2 weeks. Individuals react differently. Some
go about their usual affairs; others are comfortable in bed; others
become weak and depressed. When discomfort persists even after
habituation, and in any mild case when desirable, the ordeal is miti-
gated if possible. The addition of a few hundred grams of thrice
cooked vegetables to the bran, soup, and coffee of an ordinary fast-
day may give relief. Especially in milder cases, vegetable days are
useful; not the old fashioned kind with fat and other additions, but
only vegetables containing such carbohydrate as will not raise the
blood sugar above 0.15 per cent and will leave it not above 0.1 per
cent on the following morning. Protein and other foods necessarily
diminish the benefit of a fast-day in proportion as they are allowed.
Von Noorden's designation of fast-days as "metabolic Sundays" is
suggestive. There is no evidence whether the same number of calories
weekly will be borne any differently if distributed over 7 or 6 days.
But as the body in other respects seems to function more efficiently
by working 6 days and resting 1, it is possible that a similar prin-
ciple may apply to metabolism; also, the patient may perhaps feel
and work better if he takes the larger ration on 6 days and relaxes
as completely as necessary on the 7th. The occasional relief from the
metabolic burden may also be beneficial in even the mildest cases, in
guarding against downward progress and in atoning for any chance
indiscretions. Such days of special restriction are also a strong re-
minder of the existence of diabetes and the need of continuous precau-
tion, so that they aid instead of hindering discipline. Regular fast-
days are intended for prevention of symptoms. When fasting is
compelled by the actual occurrence of glycosuria or hyperglycemia,
the diet is wrong and must be changed. ,

152 CHAPTER n

2. Water. — There is no objection to mineral waters, but they are
without special virtues and are unnecessary when good plain drink-
ing water is available. Mineral springs and resorts should be rated
solely according to the efficiency of their dietetic treatment, and in as
far as curative influence is attributed to the water they constitute an
unfavorable environment.

3. Alcoholic Beverages. — As stated, all alcohol habits are best dis-
couraged, and as the calories of alcohol must strictly be counted in a
limited diet, the patient will generally prefer more wholesome food.
Light wines, as low as possible in both carbohydrate and calories, are
probably best for those with whom alcoholic beverages are a habit
too firmly fixed to be broken.

4. Coffee or Tea.— The use of weak tea or coffee, or Kaffee Hag, not
more than three cups daily, has already been mentioned as permis-
sible with fasting or any diet, except that a coffee habit has not been
cultivated in persons not addicted to it. Joslin often substitutes a
drink made of cocoa hulls.

5. Milk. — Sugar-free milk of satisfactory taste is prepared by
D. Whiting and Sons, 570 Rutherford Avenue, Boston, Mass., and its
keeping qualities are such that it can be shipped long distances.
Little use has been made either of it or of home-made preparations of
casein and washed cream (i.e. cream mixed with large volumes of
water to remove lactose, and skimmed off after rising or centrifuga-
tion). Milk is important for children, but it is considered the best
policy to regulate their total diet so as to create sufficient carbohy-
drate tolerance to enable them to take natural milk. Sugar-free
milk would thus be needed only temporarily, or as part of the diet of
diabetic infants.

6. Soup. — Thin soup made from bones or stock contains very little
nutrition, but its warmth and flavor are highly gratifying, and it also
supplies salts, and aids in serving bran biscuits, thrice cooked vege-
tables, and other articles having httle taste. It has been allowed in
quantities of 300 to 600 cc. daily, during fasting, carbohydrate tests,
and all other diets. Sometimes beef tea, made from beef extract,
has been used as a means of avoiding even the small quantities of
protein of ordinary soup.

GENERAL PLAN OF TEEATAIENT 153

7 . Salt. — Probably because of the rather monotonous and unsatis-
ifying diet,' patients with severe diabetes often crave surprising quan-
tities of salt. Many of them develop edema on unrestricted salt
intake. The susceptibility of individuals differs. Though no real
harm has been seen from the edema, salt-free diet has sometimes
temporarily been necessary to remove it, and for all severe cases
sodium chloride is given in a weighed daily allowance like other
items in the diet. The limit has commonly been 5 gm. daily; some-
times only 3 gm., occasionally as much as 8 gm. Numerous glass
tubes containing such weighed quantities of salt are kept on hand
in the diet kitchen. The nurse uses a part of the day's allowance for
seasoning, and the rest is placed in a small salt shaker on the pa-
tient's tray, to be used at his discretion with one day's meals. The
craving is generally not noticed when limitation of the supply pre-
vents forming the abnormal habit.

8. Meats. — Meats are included in the diet according to their food
value and the tastes and digestion of the patient. Eggs and vegetable
proteins are available on the same basis. No indications of specific
differences between proteins and no advantages in vegetarianism have
been observed. For a low protein vegetarian diet, it would be neces-
sary to use care in selecting the kinds of protein, to assure an adequate
supply of all indispensable amino-acids.

P. Fats. — These are chosen on a similar basis of suitability; There
is no need to pay attention to the content of higher or lower fatty
acids from the standpoint of ketonuria. If anything, butter is pref-
erable to olive oil.

10. Raw and Steamed Vegetables. — Since carbohydrate is desirable
in the diet, it is obviously preferable to use vegetables without ex-
traction when possible. Even ordinary boihng is a partial extraction.
Therefore, for accurately retaining the food value, vegetables have
been served either raw or steamed in the steamer above described.
Additional mention may be made of canned vegetables, which are
used either in this way or after thrice cooking if necessary. Canned
or dried vegetables are important aids to the winter diet.
Patients sometimes prepare their own supply in summer. The ad-
vantage of giving carbohydrate in the pleasant, varied, bulky, and
satisfying form of vegetables, rather than in smaller quantities of

154 CHAPTER II

bread or cereals, is obvious. With green vegetables, eggs, butter,
etc., there should be no fear of a lack of vitamines or other accessory
substances in the diabetic diet.

11. Thrice Cooked Vegetables. — ^Whatever time a vegetable requires
to cook is divided into three approximately equal periods, and the
boiling water changed so as to make three extractions of carbohy-
drate. Each patient's portion is made ready for cooking as usual,
weighed raw, and tied loosely in a single layer of cheese-cloth, and
the portions for different patients thus boiled together in one large
pot. The thrice cooked vegetables have been used to contribute
bulk with negligible food value. They are so important for this
purpose that the treatment would in some cases be almost impossible
without them, and they -add much comfort in other cases not quite
so severe. The different kinds of vegetables vary in the degree to
which they retain their flavor, but most are palatable and some are
practically as appetizing as with ordinary cooking.

Their empirical use without analyses has entailed some uncertainty
and inaccuracy in the present series. Such analyses before and after
boiling or extraction have been made by Wardall.*' There is always
a question in interpreting such figures. The cellulose of which
vegetables are largely composed is a carbohydrate, but indigestible.
On the other hand, if starch and soluble carbohydrates are alone
considered, there is a question whether other substances present may
not become potential sugar-formers upon digestion. Furthermore it
is possible that more or less starch inclosed within cellulose may not
be utilizable. Phloridzinized animals could scarcely furnish fully
conclusive results. Accordingly an empirical element remains, and
numerous patients in the present series have had sufficiently severe
diabetes that extracted vegetables could not be taken without limit.
The empirical observations have closely agreed with Wardall's chemi-
cal proof that spinach, celery, and asparagus are the safest for this
purpose. Cabbage, cauliflower, Brussels sprouts, and onions retain
enough carbohydrate to cause glycosuria much more readily than the
three first named. If only 1 per cent absorbable carbohydrate
should remain, and if a kilogram of the vegetables should be given in a

" WardaU, R. A., J. Am. Med. Assn.. 1917. box, 1859-1862. See also Joslin's
text, 2nd edition, p. 261.

GENERAL PLAN OF TREATMENT 155

day, it is clear that such carbohydrate content is important for a
patient whose actual tolerance may be 5 gm. or less. As previously
mentioned, this state of excessively low tolerance ought not to be
allowed to persist; but nevertheless carbohydrate should always be
reckoned as accurately as possible. There is no reason why patients
whose tolerance is a little greater should not, at least for occasional
variety, receive higher class vegetables which have been extracted
to reduce their carbohydrate content; but analyses such as those of
Wardall will be necessary before they can be used with accuracy.
What can be done with fruits in this direction will also bear further
investigation.

Besides a little carbohydrate, thrice cooked vegetables convey more
or less salts, and may have some real importance in this respect.
Blunt and Otis*' found that spinach loses 50 per cent, string beans
43 per cent, navy beans 39 per cent, peas 36 per cent, and potatoes
22 per cent, respectively, of their iron in cooking. Salts of potassium
and heavy metals are also furnished in utilizable form by such vege-
tables. Courtney, Fales, and Bartlett*' investigated the salt content
of vegetables boiled so thoroughly as to be comparable to the thrice
cooked kind. Tables IV and V are reproductions of two of their
tables.

This large loss of salts occurred in the first few minutes of boiling;
for example, spinach boiled only 10 minutes had already lost 42.2
per cent of its ash; the very prolonged further boiling had relatively
little effect. These authors confirm the well known marked predomi-
nance of bases over mineral acids in vegetables, and the assimilable
character of these bases, which are probably in combination with or-
ganic acids. It is possible that the very high plasma bicarbonate
(above rather than below 65 per cent) so often, found in severe cases
under rigid treatment may be attributable to the vegetable diet.
With the customary liberal use of vegetables, diabetics should certainly
suffer no lack as respects quantity, variety, or assimilability of the
supply of mineral bases.

** Blunt, K., and Otis, F. A., J. Home Economics, 1917, ix, 213-218; Chem.
Abstr., 1917, xi, 2124.

*' Courtney, A. M., Fales, H. L., and Bartlett, F. H., Am. J. Dis. Child..
1917, xiv. 34-39.

156

CHAPTER n

For practical purposes, thrice cooked vegetables (generally spinach,
celery, and asparagus) have been used in limited quantities without
any food value being reckoned for them. The protein of green vege-

TABLE IV.
Content in Gm. of Solids of 100 Gm. of Vegetables Erepared by Boiling.

Vegetable.

Spinach. .
New-
Zealand
spinach.
Young. . .
carrots
Onions.. .
String

beans. .
Aspara-
gus. . . .
Potatoes.

90

30

30

45

ISO

30
30

Solids.

.30

4.26

6.31
6.82

5.31

4.59
20.51

Ash.

1.172

0.535

0.408
0.398

0.371

0.370

CaO

0.305

0.145

0.039
0.020

0.070

0.038

MgO

0.035

0.021

0.014
0.013

0.030

0.021

PjOb

0.123

0.052

0.043
0.067

0.063

0.101

CI

0.036

0.000

0.023
0.008

0.045

0.024

KsO

0.238

0.157

0.181
0.186

0.123

0.174

NaaO

0.068

0.040

0.038
0.010

0.011

0.001

HjSOi

0.034

0.016

0.022
0.056

0.025

FezOj

0.0090

0.0154

0.0070
0.0026

Tr.

0.497

0.236

0.108
0.189

0.190

0.283

i

3 1

3.10

1.48

0.67
1.18

1.19

1.77

TABLE v.
Percentage Lost in Water under Ordinary Boiling Conditions.

Vegetable.

3

JZ

^

9

61.5
81.0
41.6
10.6
54.1
40.1

2

o

<2

9

61.1
77.8
48.8
0
56.3
Tr.

57.2
78.7
49.9
31.6

52.1

6

28.2
50.8
Tr.

U

Tr.

a;

Sninacli . , ;

90
30
30
45
150
30
30

32.2
41.3
37.5
22.5
31.8
27.4
4.4

45.2
72.2
47.8
28.0
43.4
46.7

Tr.

3.6
28.4
26.1
21.4
26.6

48.2
70.2
34.6
24.6
42.7
34.6

71.1
100.0
57.1
31.4
46.8
46.4

64.8
81.9
47.3
29.2

55.2
49.2

?3 1

New Zealand spinach.. . .
Youner carrots

22.3

?? 7

Onions

19 8

Striner beans

?6 7

Asnaraffus

?4 1

Potatoes

tables is known to be poorly absorbable.^" Irrespective of any food
content, diabetics should not be allowed to gorge themselves on these
extracted vegetables. Those on reasonably liberal diets do not need
them at all. The allowance for any patient is generally not more

5" Rubner, M., Berl. klin. Woch., 1916, No. 15.

GENERAL PLAN OF TREATMENT 157

than a kilogram per day, and less in proportion as ordinary vegetables
can be used. Excessive quantities are a useless burden upon both
the purse and the digestion.

12. Fruits. — Fruits are the best diabetic desserts, when they can be
tolerated. Most patients can take at least grape-fruit. Within
reasonable limits, there is no prejudice against fruits because of their
carbohydrate being largely in the form of sugar. Neither is there a
favorable bias because so much of the sugar is levulose, for in the long
run the actual carbohydrate and total food values are probably the
determining factors of a diet. Reference must be made to text-books
for the proportions of different carbohydrates in fruits. The latest
article that has chanced to come to notice is that of Eofi," showing
that 52 to 75 per cent of the sugar in apple juice is levulose.

13. Nuts. — Some nuts resemble prepared diabetic foods in their low
carbohydrate and high protein and fat content. They must be used
with corresponding caution. No superior assimilation for nuts or
other less common foods has been observed.

14. Unusual Carbohydrates and Abnormal Modes of Administration. —
Notwithstanding more or less deceptive appearances of assimilation,
little or no practical value is to be expected from caramel, pentose,
7-carbon sugars (hediosit), or other unusual food elements. Like-
wise no hope should be entertained of any special assimilability of
glucose given by rectum or other abnormal way. It need only be
noticed that no patient was ever saved from either starvation or coma
by such means. Confusion will be avoided by recalling the faulty
theory underlying such attempts. In acidosis, the only lasting benefit
must come from relief of the metabolism which is breaking down, by
reducing the diet especially in fat, and not from the introduction of
strange compounds. In nutrition, the level of total diet and weight
determined by the actual assimilative power is a limitation which
cannot be cheated by artificial devices.

15. Bran Bread or Biscuits. — These are the only form of bread
substitute used for the type of cases treated in this hospital. In
milder cases bran can be used in various ways; for example, bread can
be made of eggs, fat, and bran, or bran can be mixed with ordinary

" Eoff, J. R., J. Ind. and Eng. Chem., 1917, ix, 587-588.

158 CHAPTER n

flour to lower the carbohydrate and food value of the latter. But
while severely diabetic patients crave some form of bread, they do not
wish to devote any of their scanty protein or fat to this use. Accord-
ingly the following recipe was developed for a bran-agar bread
having no appreciable food value.

Bran Biscuits.

Bran, weighed dry 60 gm.

Agar-agar, powdered 6 "

Cold water ; 100 cc.

The bran is tied in cheese-cloth and hung under the cold water tap
to wash (with stirring or kneading as required) until the water
runs through clear. The agar is mixed in 100 cc. water (cold) and
brought to the point of boiling. The agar solution (hot) is then
added to the washed bran. The mixture is molded into three cakes
and placed in a pan and when firm and cold baked until dry and crisp.
Salt may be included in the recipe if desired. The biscuit or muffin
shape may be chosen, but it has generally been preferred to make thin
flat pieces like well browned toast. The toasting helps the flavor a
little, and the dryness facilitates keeping.

The chief caution is necessary in the choice of bran. Ordinary bran
flours or breakfast foods are high in carbohydrates. Some kinds of
cheap bran contain middlings or other carbohydrate admixture. It is
possible to buy purified bran, such as Kellogg's. But the bran
ordinarily used for feeding cattle, which on inspection is seen to con-
sist of coarse flakes of the outermost hull of the wheat, is obtain-
able very cheaply at feed stores, and is perfectly satisfactory when
washed under the cold water tap for half an hour or more as above
described.

Some patients like these tasteless bran rusks at once; others either
accept or enjoy them after becoming used to them. They are best
served hot, like toast, with butter, bacon fat, a fried egg, or even
soup, to give them flavor. Besides contributing bulk, like the vege-
tables, the bran is stiU more active in favoring catharsis, and since its
introduction the traditional constipation of diabetic patients has
been almost unknown in this hospital. A few individuals cannot
take the bran; in others sometimes indigestion or diarrhea limits the

GENERAL PLAN OF TREATMENT 159

amount. On general principles, an inert substance should not be
taken to excess, and accordingly the allowance is generally no more
than one or two of the above cakes at each meal.

Bran has never been responsible for glycosuria in this hospital,
and is probably not digested to any important extent. The chemis-
try of bran, especially from the standpoint of digestion, is not thor-
oughly known. It is poor in cellulose (2 to 4 per cent in most analy-
ses), and from its richness in protein and amides, phytin and other
complex compounds, might supply the body with much nitrogen and
phosphorus if digestible. Guareschi^^ states that bran milled to an
impalpable powder is 91 to 92 per cent digestible, and emphasizes its
value for food and for vitamines. The fine milling therefore defeats
the purpose for which bran is used in diabetes.

16. Proprietary Foods. — So called "diabetic" and "gluten" prepa-
rations have largely fallen into disrepute because of the rankly fraudu-
lent character of so many of them. It is still very common for pa-
tients to announce that as soon as diabetes was discovered they be-
gan to eat gluten bread, with or without a doctor's orders; but knowl-
edge on the subject is increasing, and it is becoming generally known
that a physician should at least never order such a food without
specifying a reliable brand.

The medical profession is indebted to Professor John P. Street for
the most complete analyses of diabetic foods. The results are obtain-
able in the publications of the Connecticut Agricultural Experi-
ment Station, especially the report for 1913, Part 1, with added analy-
ses in the report for 1914, Part 5, and the report for 1915, Part 5.
These data are the best basis for the choice of a diabetic preparation.
With improved technical methods, the best brands have been brought
to a high state of perfection from the standpoint of carbohydrate-
ireedom and agreeable taste. Without invidious distinctions, men-
tion may be made of American made examples of the three principal
classes of such foods; viz., gluten flour, which is manufactured in high
purity by Hermann Barker, Somerville, Mass.; casein flour and
muflSns, as prepared by Lister Brothers, 110 West 40th Street, New

^^ Cf. Guareschi, I., Ind. ckim., min. e metal.; 1917, iv, 97-103; Chem. Abstr.,
1917, xi, 2124. Holmes (Holmes, A. D., U. S. Dept. Agric, Bull. 751, 1919) has
obtained a coeflScient of digestibility of only 45 per cent for finely milled bran.

160

CHAPTER n

York City; and soy bean flour, one brand of which is made by the
Cereo Company, Tappan, New York, while the most extensive use
of soy beans by diabetics at present is in the form of the "Hepco"
flour, dodgers, etc., made by the Waukesha Health Products Com-
pany, Waukesha, Wisconsin. For complete hsts and analyses of such
foods, reference must be made to Street's reports or Joslin's text-book.

The essential objection to all such bread substitutes is that in ab-
sence of carbohydrate, they have necessarily been composed of pro-
tein and fat, and thus have represented highly concentrated forms of
food. Both physicians and patients have often viewed these breads
as harmless, or even commendable by reason of their high protein and
food value. The great amount of protein and calories that can be sO'
easily and inadvertently consumed in this way is capable of tre-
mendous damage. Janney^' has pointed out that the potential car-
bohydrate represented in the protein often exceeds the total carbohy-
drate of ordinary bread. It is necessary to warn strongly against this-
indiscriminate misuse of even the best preparations, in which the
manufacturer is not to blame. There is no objection to making upi
as large a proportion of the diet as desired from these flours, provided
the total diet is accurately reckoned and restricted as usual. For cases,
of the grade of severity treated in this hospital, the use of such prepa-
rations has been abandoned, simply because the patients prefer to
take their protein and fat in meat, eggs, bacon, butter, etc., rather
than in flour or bread.

Because of the very limited quantity of these concentrated foods-
which can safely be included in any diet, and because of the danger-
ous ease with which patients can be tempted to overstep their real
tolerance by taking only a small quantity in excess, the manufacturers-
of some of the better brands are moving in the direction of reducing;
the undesirably high food value by the introduction of some indigesti-
ble substitute for carbohydrate. A non-utilizable flour might be
employed in three ways; first, to dilute ordinary flour for mild cases,
so as to reduce the carbohydrate and food value of wheat, corn, or
other bread; second, to dilute the special diabetic flours, so as to make
them permissible more often and in larger quantities, Fhile at the same-

" Janney, N. W., Arch. Int. Med., 1916, xviii, 584-605.

GENERAL PLAN OF TREATMENT 161

time probably reducing their cost; third, for making an entirely non-
nutritious bread substitute, perhaps finer and more agreeable than the
bran bread. An extreme illustration of the feasibility of the use of a
non-nutritious flour can be gained by making a batter with egg, spices,
and impalpable talcum powder, and frying it crisp. This will appear
more satisfying than the egg fried alone. While talcum is inert and
harmless, it is scarcely to be recommended for eating, and a non-
utilizable flour for practical use is most likely to be found in the
vegetable kingdom, probably in some form of cellulose or other
polysaccharide.^* Ridicule or opposition may be aroused by sug-
gestions of flour from cotton, peanut-shells, corn-pith, etc., and the
technical difficulties also have thus far baffled manufacturers. The
German experience in the recent war, that large quantities of wood
flour may cause intestinal disturbance, was confirmed in one short test
with diabetics; but the long experience with bran and shorter trials of
other indigestible substances have shown that the prudent use of these
is safe and practicable. Critics should bear in mind the following
facts: first, it is generally conceded that the food of civilized man is
overconcentrated, frequently excessive, and subject to improvement
by an admixture of indigestible material, as in coarse vegetables;
second, the diabetic flours which it is proposed to dilute are dry pro-
tein-fat powders representing an unnaturally concentrated form of
food; third, diabetics must be more closely limited in their total food
intake than normal persons, and yet they have the usual, even if not
an excessive craving both for bread and for bulk.

D. General Scheme and Specimen Diets.

Two general plans, are possible for diabetic diets. The one which
has been customary in the past has aimed to give the patient substi-
tutes as nearly as possible resembling the accustomed dishes which
he must forego. Accordingly, diabetic cook-books have been fflled

^* Concerning some indigestible carbohydrates, see Mendel, L. B., Ceniralbl.
ges. Physiol, u. Path. Stoffwechs., 1908, iii, 641-654. Mendel, L. B., and Swartz,
M. D., Am. J. Med. Sc, 1910, cxxxix, 422^26. Swartz, M. D., Tr. Connecticut
Acad. Arts, and Sci., 1911, xvi, 247. Concerning the German experience with
wood flour, see Salomon, H., Wien. med. Woch., Dec. 15, 1917 (favorable), and
Neumann, R. O., Vrtljschr. gerichll. Med., 3rd edition, li, pt. ii, (unfavorable).

162 CHAPTER II

with composite recipes, carbohydrate-free puddings, saccharine sweet-
ening, imitation milk, and a host of similar artifices. The most con-
venient way to manage such a diet accurately is to weigh out the
day's allowance of eggs, fat, etc., in the morning and use for cooking
the different meals as required. It may be urged that habits of food
are hard to break, and that a diabetic should not be deprived of
gustatory pleasure xmnecessarily. It may be objected on the other
hand that such diets tantalize and tempt more than they satisfy;
that saccharine keeps aUve the taste for sugar, that the liabiUty to
carelessness is increased, and that a patient does best to face squarely
the fact of his diabetes and the necessary restrictions, and to resolve
to eat to hve rather than Uve to eat, especially since care in diet is the
means whereby all the other pleasures and advantages of the world
are opened to him in fullest measure.

It is generally beheved that the plainest and simplest diets are the
most wholesome for mankind in general. It has therefore been consid-
ered inadvisable to take such great pains to depart from such a diet
for diabetics. Not only is simpHcity highly important for accuracy,
fidehty, convenience, economy, and healthful habits, but in the long
run the simple diet has proved the most satisfying and the least irk-
some. The patient begins such a Spartan regime immediately after
his initial fast in the hospital, when anything tastes good, and by the
time he leaves the hospital his new habit of diet is estabhshed. With
simple menus and a balanced ration, diabetics are free from abnormal
cravings, and natural himger on reduced diets is also easier to appease.

Simplicity does not mean unpleasantness to sight or taste. Here the
skill of the diet nurse or cook comes into play. The refinement of
the table service, even though not expensive, has its esthetic value.
Salads and other simple dishes can be made attractive in appearance.
A single egg can loom surprisingly large to the eye if beaten into a
fluffy omelette or souffle. Variety in cooking and combining the
same foods varies them to the taste. Vegetables offer variety in soups,
and the different ways of serving meat are well known. Eggs, bacon
grease, meat, or the juice from meat give variety and taste to thrice
cooked vegetables, and even to bran muffins. There is no inherent
objection to condiments or spices, but these, except salt, have been
little used, since the diabetic appetite generally needs no stimulation,

GENERAL PLAN OF TEEATMENT 163

and the simple taste of plain foods is sufl&ciently appreciated. Coffee
lovers generally learn readily to like their drink black, without sac-
charine. A little fruit is a sufficient dessert in most cases. The de-
sire for cake, puddings, and other luxuries is discouraged by disuse.
Exceptions have been made only in some extremely severe cases on
minimal diets, since small treats mean so much to these patients.
Agar jelly, ices, sherbets, etc., can be flavored with saccharine, coffee,
wine, brandy, fruit juices, or sugar-free caramel (the quantities re-
quired being very small). Likewise agar with soup or beef extract
makes an agreeable meat jelly. Such tricks often eke out a low diet
or reheve a hard fast-day in the worst cases; but the better fed class
of patients do not need them.

The physician who cannot calculate diets to suit his individual cases,
but is dependent upon text-book menus, will not be able to substi-
tute celery or spinach when one or the other is disliked, and will oc-
casionally meet patients who know more about diets than he. Any-
body who has a list of food values and can use the decimal system can
easily make up the simple diets required by diabetics. The unwise
complexity of dishes in the past has doubtless been largely respon-
sible for the unfortunate helplessness of so many physicians in this
regard. The use of the metric system is not a difficulty but a great
convenience, and it can be learned in a few minutes by those un-
accustomed to it. Though the energy value of carbohydrate and pro-
tein is 4.1 calories per gm., and of fat 9.3 calories per gm., it is suffi-
ciently accurate for ordinary purposes to reckon them as 4 and 9
calories respectively.^^ One elementary example should make the
method clear. .

Suppose that a patient's weight is 50 kilograms, that his tolerance
in the carbohydrate test was 180 gm., and that he is to be given a
mixed diet containing one-sixth of this maximal carbohydrate toler-
ance, together with 1.5 gm. protein and 30 calories per kilogram.

^^Food chemists are well aware of the technical considerations which make
absolute exactness impossible in the ordinary reckoning of a diet. A practical
point is that the number of calories obtained by multiplying the total grams of
protein, carbohydrate, and fat by the proper factors, and the number found by
adding up the calories given in food tables for the individual meats, vegetables,
and other foods served, are seldom identical. Either method is permissible.

164

CHAPTER n

One-sixth of the carbohydrate tolerance of 180 gm. is 30 gm. Any
desired vegetables are selected from food tables to make up this total
of 30 gm. for the day, and divided between the meals at will. The
protein, fat, and calories in the vegetables chosen must be reckoned,
which will give a result such as shown in Table VI.

TABLE VI.

Food.

Carbohy-
drate.

Protein.

Fat.

Breakfast.

Canned asparagus

gm.
150

50

37
148
142

50

150

86

gm.

4.2

1.7
1.1

5.0

5.5

1.7
5.9
5.0

gm.
2.3

0.7
0.5

2.2

1.1

0.7
1.2
1.4

gm.

0.2

0.2

0.1
0.5

0.2
0.6
0.6

Dinner.

Lettuce

Celery

Canned Brussels sprouts

Raw tomato

Supper.

Lettuce

Raw tomato

Cauliflower

Gm

30.0
120.0

10.0
41.0

2.4
22.3

Calories

18"?

TABLE VII.

Food.

Protein.

Fat.

Breakfast.

Eggs

gm.

100
50

57
25

100
50

gm.

14.8
5.0

18.3
6.5

14.8
5.0

gm.

10.6
33.6

2.5
7.9

10.6
33.6

Bacon

Dinner.

Roast chicken

Cream cheese

Supper.

Eggs

Bacon

Gm

64.6
258.0

98.8
899.0

Calories

1157.0

GENERAL PLAN OF TREATMENT

165

Taking up next the protein allowance, this, at l.S gm. per kilogram
for a weight of SO kilograms, will amount to 75 gm. of protein. Since
10.4 gm. of protein is contained in the vegetables already chosen,
this leaves 64.6 gm. yet to be supplied for the day (Table VII).

TABLE

VIII.

■

Food.

Carbo-
hydrate.

Protein.

Fat.

Bueakfast.

Eess

gm,

100

50

ISO

5

57
10
50
37
148
142
25

100

50

9

50

150
86

cc.

150
150

150
150

150
150

4.2

1.7

1.1

5.0

5.5

1.7
5.9
5.0

gm.

14.8
5.0
2.3

18.3

0.7
0.5
2.2
1.1
6.5

14.8
5.0

0.7
1.2
1.4

gm.

10.6

33.6

0.2

4.1

2.5
8.2
0.2

0.1

0.5
7.9

10.6
33.6
7.4
0.2
0.6
0.6

Bacon

Canned asparagus

Butter

Bran biscuits (2)

Coffee

Clear soup

Dinner.

Roast chicken

Butter .

Lettuce

Celery

Canned Brussels sprouts

Raw tomato

Cream cheese

Bran biscuits (2)

Kaffee Hag.

Clear soup

Supper.

Eggs

Bacon

Butter . .

Letituce

Raw tomato

Cauliflower

Bran biscuits (2)

Kaffee Hag

Clear soup

Gm

30.0
120.0

75.0
300.0

120.6
1085.0

1505

A ration of 30 calories per kilogram for a weight of 50 kilograms
means 1500 calories for the day. Since the foods chosen for carbo-
hydrate and those chosen for protein together represent 180+1157 =

166

CHAPTER n

1337 calories, this leaves 163 calories yet to be supplied in the fonn of
fat. It is now necessary to divide the 163 calories by 9, thus showing
18 gm. as the quantity of fat needed. This could be supplied by 18
gm. of olive oil, or 24 gm. of butter, or the equivalent in any other
fat. The total diet for the day is shown in Table VIII.

The specimen diets in Tables IX to XV are given as suggestions.
In them, the factors 4.1 and 9.3 are used, as customary in this
hospital.

TABLE rx.

Carbohydrate Tolerance Test.

A Day's Diet with 30 Gm. Carbohydrate.

Food.

Breakfast.

Canned asparagus

Coffee

Clear soup

Dinner.

Lettuce

Celery

Canned Brussels sprouts.

Canned okra

Clear soup

Kaffee Hag.

Supper.

Lettuce

Raw tomato

Spinach

Canned okra

Clear soup

Kaffee Hag.

m

Calories.

ISO

25

75

150

65

25
ISO
200

66

150
150

150
150

150
150

FFotein.

2.3

0.4
1.0
2.2
0.4

0.4
1.2
4.2
0.5

12.5
51.0

Fat.

0.2

0.1
0.1

o:o5

0.1
0.6
1.0
0.05

2.2
20.0

Carbo-
hydrate.

4.2

0.9
2.2
5.1
2.3

0.9
5.9
6.2
2.4

30.0
123.0

194

GENERAL PLAN OF TREATMENT

167

TABLE X.

Carbohydrate Tolerance Test.
A Day's Diet with 100 Gm. Carbohydrate.

Food.

Breakfast.

Canned asparagus..

Beets

Celery

Clear soup

Coffee

Dinner.

Lettuce

Raw tomato

Carrots

Cabbage

Clear soup

Canned okra

Celery

Kaffee Hag

Supper.

Lettuce

Celery.

Turnips

Clear soup

Canned okra

Raw tomato

KaSee Hag

gm.

ISO

208

SO

100
203
218
172

90
SO

SO
100
230

90

S4

ISO
ISO

150

ISO

ISO

150

Gm

Calories.

Protein.

gm.

2.3
3.2
0.7

1.3

1.6

2.3
3.5

0.7
0.6

1.5
1.4
3.2

0.6
0.4

23.3
95.5

Fat.

Carbo-
hydrate.

gm.

0.2
0.2
0.05

0.4
0.8
0.8
0.6

0.1
0.05

0.2
0.1
0.4

0.1
0.2

4.3
45.6

gm.

4.2

20.0

1.5

3.3

7.9

20.0

10.0

3.2
1.5

1.7

3.0

20.0

3.2
2.1

101.6
416.6

557.7

168

CHAPTER n

TABLE XI.

Carbohydrate Tolerance Test.
A Day's Diet with 250 Gm. Carbohydrate.

Food.

Breakfast.

Orange

Canned peas

Carrots

Rice

Coffee

Clear soup

Dinner.

Grapefruit

Lettuce

Canned asparagus..

Potato

Canned lima beans.

Turnips

Kaffee Hag

Clear soup

Supper.

Apple

Lettuce

Raw tomato

Parsnips

Onions

Kaffee Hag

Clear soup

104

204

218

39

200
100
ISO
168
205
230

120
100
64
122
303

150
150

150
150

150
150

Gm

Calories .

Protein,

gm.

0.8

7.2
2.3
3.0

1.3
2.3
2.0
8.2
3.2

0.6i
1.3
0.5
2.0
5.1

Fat.

39.8
159.1

gm.

0.6
0.4
0.8
0.1

0.4
0.2
0.1
0.6
0.4

0.6
0.4
0.2
0.6
1.2

6.6
61.4

Carbo-
hydrate.

gm.

10.0
20.0
20.0
30.0

10.0
3.3
4.2
30.0
30.0
20.0

20.0

3.3

2.5

19.6

30.0

252.9
1025.0

1246

GENERAL PLAN OF TREATMENT

169

TABLE XII.
Exclusive Protein Diet, as Sometimes Used for Bringing Down Blood Sugar.

Food.

Breakfast.

Egg white

Celery T.C.*

Spinach "

Coffee

Clear soup

Bran biscuits (2)

Dinner.

Flounder

Sauerkraut T. C

Brussels sprouts T. C.

Bran biscuits (2)

Coffee.

Soup

Supper.

Roast chicken

CauHflowerT. C

Asparagus "

Bran biscuits (2)

Kaffee Hag

Soup

Gm

Calories.

gm.

162
200
100

216
200
200

78
200
100

150
ISO

150
150

150
150

Protein.

20.0

30.0

25. 0

75.0
307.0

Fat

0.3

1.2

3.4

4.9
45.0

352

' T. C. indicates thrice cooked.

170

CHAPTER n

TABLE Xni.

Example of a Low Maintetiance Diet for a Case of Extreme Severity; Body Weight

30 to 40 Kilograms.

Food.

Bieakfast.

Eggs

Bacon

Butter.

Celery T.C

Bran biscuits (2).. ,

Coffee

Clear soup

Dinner.

Flounder.

Butter

Lettuce

Raw tomato

Cauliflower T. C. .

Asparagus " . .

Bran biscuits (2)...

KaffeeHag

Clear soup

Sup per.

Eggs

Cream cheese

Butter.

Lettuce

Canned asparagus..

Spinach T.C

Cabbage "

Bran biscuits (2) . .

Kaffee Hag

Clear soup

Gm

Calories.

gm.

100

50

7

200

72

7

25

34

200

200

100

13

7

25

71

200

200

150
150

Protein.

150
150

150
150

14.9
5.0

10.0

0.4
0.2

14.9
3.3

0.4
1.0

50.1
205.0

Fat.

gm.

10.6

33.6

5.8

0.4
5.8
0.1
0.1

Carbo-
hydrate.

10.6
4.1
5.8
0.1

77.0
716.1

gm.

0.9

1.3

0.9
2.0

5.1
21.0

942

GENERAL PLAN OF TREATMENT

171

TABLE XIV.

Specimen Diet of a Child Aged 3 or 4 Years {Patient No. 73), with Extremely Severe
Diabetes; Weight 9 Kilograms.

Food.

Protein,

Fat.

Carbo-
hydrate,

7:30 a.m.

Egg

Milk

Butter.

Asparagus T. C...

Clear soup.

Bran biscuit (1)

11:00 a.m.

Egg.

Milk

Canned asparagus..

Butter.

Clear soup.

1:00 p.m.

Milk

Butter.

Raw tomato

Clear soup

Bran biscuit (1).. . .
3:00 p.m.

Milk

Clear soup

5:30 p.m.

Egg.

Milk

Butter.

Celery.

Bran biscuit (1)....

Clear soup

SO
25

7
75

50

25

107

6

50

6

60

25

50
25

7
75

100

100

100

100

100

Gm

Calories.

(m.

7.4
0.8

7.4
0.8
1.6

1.6
0.5

0.8

7.4
0.8

1.0

30.1
125.0

gm.

5.3
1.0
5.8

5.3
1.0
0.1
4.9

2.0
4.9
0.2

1.0

5.3
1.0

5.8

43.6
405.0

1.3

1.3
3.0

2.5
2.3

1.3

1.3

2.2

15.2
62.3

591

172

CHAPTER n

TABLE XV.

Example of a Maintenance Diet, Showing the Substitutions Indicated for Patients Who

Cannot Perform Calculations for Themselves.

Protein 90 gm. Carbohydrate 50 gm. Calories 2000.

Food.

1

i

V

1

Substitutes.

gm.

cc.

gm.

gm.

gm.

Breakfast.
Eggs

100
50
13

ISO

96

20
•25
150

295

100

19

100
SO
20
25
75
323
172
19

ISO
LSO

150
150

ISO
150

14.8
5.0

2.3

22.3

0.4
1.2

4.4
1.6
4.9

14.8
5.0

0.4
1.0
6.7
3.5
4.9

10.6

33.6

10.7

0.2

1.5

16.5
0.1
0.6

0.3
0.8
6.0

10.6

33.6

16.5

0.1

1.6
0.6
6.0

4.2

0.8
5.9

10.0
6.0

0.8

2.2

10.0

10.0

Bacon

Butter

Canned asparagus.
Bran biscuit (2)...
Coffee

Fresh asparagus 124 gm. (in place of canned).

Clear soup

Dinner.

Roast beef

Butter.

Roast chicken 69 gm.less butter 2 gm.

Flounder 160 gm.

Veal 79 gm.

Roast Lamb 113 gm. less butter IS gm.

(in

place of

roast

beef).

Radishes 25 gm. (in place of lettuce).

Raw tomato

Canned Brussels

sprouts

Cauliflower

Cream cheese

Bran biscuits (2) . .

Kaffee Hag

Clear soup

Supper.

Beets 61 gm. (in place of tomato).

Carrots 109 gm. (in place of Brussels sprouts).

Celery 200 gm. (in place of cauliflower).

Bacon

Butter

Lettuce

Celery

Dill pickle 82 gm. (in place of celery).

Spinach

String beans 107 gm. (in place of spinach).

Cabbage

Turnips 115 gm. (in place of cabbage).

Cream cheese

Bran biscuits (2)..

Kaffee Hag

Clear soup

Sauerkraut 228 gm. (in place of cabbage).

Gm

93.2
369.0

149.9
1394.1

50.0
205.0

Calories

1968

ClSRBiGHTDRATE

GENERAL PLAN OF TREATMENT 173

E. Food Tables.

The accompanying graphic charts illustrate a short method for
approximating food values, which can be made both more convenient
and more accurate if enlarged and used for wall charts. The abscissa
represent grams of foodstuffs; the ordinates show both grams and cal-
ories of carbohydrate, protein, and fat respectively. Thus, taking
the number 50 at the bottom of the carbohydrate chart, and follow-
ing the line up to where it cuts the line for sauerkraut, it is seen at a
glance that 50 gm. of sauerkraut contain 2 gm. or 8.2 calories of car-
bohydrate. Conversely, if it is desired to select food containing 5 gm.,
of carbohydrate, one may start at the number 5 on the left of the chart
and by following it across may see that this quantity is represented
in about 51 gm. of onions, about 67 gm. of blackberries, about 100
gm. of either grapefruit or milk, etc. The same method is used in
finding protein and fat values in the other charts.

The food values in Tables XVI to XIX are taken almost entirely
from the tables of Bryant and Atwater, Bulletin 28, Department of
Agriculture, Bureau of Experiment Stations, Washington, D. C. Simi-
lar tables, along with analyses of cooked foods, etc., are given in the
book on "Food Values," by Edwin A. Locke, Appleton and Company,
1914.

Abundant data for diabetic needs are contained in Joslin's text-
book. The list given in Chart 1 and Tables XVI to XIX is not
extensive, but yet contains nearly everything found necessary for
the diets in this hospital. Copies are supplied to patients for
reckoning their diets at home.

174

CHAPTER n

TABLE XVI.

Meat and Fish*

Edible portion.

Protein.

Fat.

Carbohy-
drate.

Meats.

fer cent

10.0
20.5
20.8
22.8
20.2
19.5
19.7
19.1
21.0

18.8
19.0
15.8
13.9
18.3
20.6
20.9
18.6

per cent

67.2

6.4

5.8

1.8

20.8

14.4

19.0

12.4

3.6

0.5
1.2
0.4
0.6
5.2
12.8
3.8
9.5

per cent
0

Beef sirloin verv lea,ii

0

" round " "

0

0

0

0

" loin . ...

0

Lamb

0

Veal

0

Fresh fish.

Sea bass

0

Blue fish

0

Cod, fresh

0

FlouiMier

0

Halibut

0

0

Shad roe

2.6

" whole :

0

*Uncooked values.

GElsTERAL PLAN OF TREATMENT

175

TABLE XVII.
Vegetables, in Order of Their Carbohydrate Content from Lowest to Highest.

Edible portion.

*Mushrooms (range 2 to 18 per cent) .

Cucumbers, fresh

Asparagus, canned

Celery, fresh

Spinach "

Asparagus "

Lettuce " !

Brussels sprouts, canned

Rhubarb, fresh

Tomatoes "

" canned

Brussels sprouts, fresh

Sauerkraut

Artichokes, canned.

Leeks

Eggplant, fresh

Pumpkin "

Cucumber pickles

Kohlrabi, fresh

Cabbage

Cauliflower

Radishes

Turnips

Carrots

Beans, string, fresh

Beets, fresh

Peas, green, canned

Onions, fresh

Squash "

Lima beans, canned

Com, green, fresh

Peas " "

Parsnip, fresh

Artichoke "

Potatoes "

Lima beans "

Protein.

Fat.

Carbohy-
drate.

per cent

per cent

per cent

(3.5)

(0.4)

(6.0)

0.8

0.2

2.5

l.S

0.1

2.8

1.4

0.1

3.0

2.1

0.5

3.1

1.8

0.2

3.3

1.3

0.4

3.3

1.5

0.1

3.4

0.6

0.7

3.6

0.8

0.4

3.9

1.2

0.2

4.0

4.7

1.1

4.3

1.5

0.8

4:A

0.8

0.2

5.0

1.2

0.5

5.8

1.2

0.3

5.1

1.0

0.1

5.2

0.5

0.5

5.4

2.0

0.1

5.5

2.1

0.4

5.8

1.6

0.8

6.0

1.4

0.1

6.6

1.4

0.2

8.7

1.4

0.4

9.2

2.2

0.4

9.4

1.6

0.1

9.6

3.6

0.2

9.8

1.7

0.4

9.9

1.6

0.6

10.4

4.0

0.3

14.0

2.8

1.1

14.1

4.4

0.5

16.1

1.7

0.6

16.1

2.6

0.2

16.7

2.1

0.1

18.0

7.1

0.7

22.0

* Wardall, (/. Am. Med. Assn., 1917, kix, 1859-1862) pointed out that the
carbohydrate of ordinary mushrooms is in some non-extractable form, and the
nitrogen according to Mendel's analyses is likewise in non-protein, non-utilizable
compounds. The figures in the above table are therefore placed in parentheses
to indicate their misleading nature. It would appear that ordinary mushrooms
may be reckoned as having no appreciable food value, and that they therefore
mav be a welcome feature of the diabetic diet.

176

CHAPTER II

TABLE XVin.

Fruits, In Order of Their Carbohydrate Content, from Lowest to Highest.

Edible portion.

Protein.

Fat.

Carbohy-
drate.

Grapefruit

per cent

0.3
1.0
0.9
0.6
0.7
0.4
0.8

0.5
1.0
1.0
1.1
0.6
0.5

per cent

0.1
0.1
0.2

0.1
0.3
0.6

0.7
1.0
1.3

0.8
0.5

per cent
5.0

Watermelon.

6.5

Strawberries

6.8

Blackberries

7.5

Muskmelon

9.3

Peaches

9.4

Pineapple

9.7

Orange

9.7

Lemon juice

9.8

Cranberries

10.1

Raspberries

12.6

Grapes

13.3

Apricots

13.4

Pears

14.2

Apples

16.6

TABLE XIX.
Dairy Products.

Edible portion.

Protein.

Fat.

Carbohy-
drate.

Eggs.

per cent
14.9

3.3
3.0
5.97
2.5

37.1
28.2
26.9
25.9
28.8
29.6
23.0
15.4
27.6
15.9
18.7
22.6

per cent

10.6

82.4
4.0
O.S
7.36

18.5

17.7
32.0
31.6
31.7
36.2
38.3
29.4
21.7
34.9
21.0
27.4
29.5

per cent

Butter

Whole milk

5 0

Buttermilk

4 8

Whiting's milk*

Cream, average

4 5

Cheese.

Dutch

Cheddar

Cheshire

Cream

American, pale

" red

Limburger

0 4

Boudon

0.7
1 ^

Swiss

Brie

1 4

Neufchatel

1 5

Roquefort

1.8

' D. Whiting and Sons, 570 Rutherford Avenue, Boston. Mass.

CHAPTER III.
Case Records.

Seventy-six cases have been selected for publication, for reasons
stated in Chapter VII. Graphic charts have been chosen as the
clearest and most compact means of presenting the large mass of
clinical and chemical data. With a little attention to the key shown
on all the charts, it is beheved that they will be found simple and
self-explanatory. The curves of ammonia, total acetone, and total
acidity of the urine have been plotted as cubic centimeters of deci-
normal solution, for the sake of chemical calculations and comparisons.
This plan will doubtless prove somewhat confusing to many clinicians,
but the tables and summaries in the case histories express the results
in grams. The written history of each case is supposed to be followed
in conjunction with the graphic chart, and reference from one to the
other will be necessary to make both plain.

Table I is a general summary of the entire series. The data mostly
tell their own story. Further details, of the age incidence, complica-
tions, results of treatment, etc., are shown in Chapter VII. The
etiologic relations are discussed in Chapter VIII.

CASE NO. 1,

Female, unmarried, age 28 yrs. American; no occupation. Admitted Feb.
24, 1914.

Family History. — Grandparents lived to healthy old age. Father living, aged
58, has arterial hjT)ertension, neuralgia, and tendency to melancholia. Mother
died at birth of this patient. An uncle died of tuberculosis. One fuU brother of
patient died at 16 of appendicitis. One half-sister aged 22 has nephritis, conse-
quent upon scarlatina.

Past History. — No childhood diseases except measles and one dysenteric attack.
Normal menstruation began at 13. Patient graduated from university at 20.
She has had a nervous, overactive life with late hours and irregular eating. Was
considered remarkable among her family and friends for the amount of candy
and sweets she consumed. Normal weight 115 to 120 pounds. July, 1912, pa-
tient's fianc6 died of accidental poisoning. Patient became melancholic and kept

177

178 CHAPTER in

more to herself, while eating still more candy than usual. She and her parents
were inclined to attribute onset of diabetes to grief.

Present Illness.— In Jan., 1913, abnormal thirst was first noted. In Mar.,
pruritus vulvae. In May, menstruation stopped and remained absent. Hair
fell out and is still thin. July, 1913, diagnosis of diabetes was made and routine
diet prescribed, which was taken in huge quantities owing to polyphagia. Symp-
toms persisted and increased till Jan. 4, 1914, when she began treatment at a
well known diabetic sanitarium. Qualitative and quantitative restriction of the
diet, oat cures, vegetable days, etc., failed to clear up the condition. She was
then transferred to this hospital, and arrived tired but not dangerously exhausted
after a journey of 32 hours.

Physical Examination.— Height 165.6 cm. Weight 40.1 kg. Marked emacia-
tion, face flushed and slightly pufiEy, drowsy and slightly alcoholic expression.
No enlargement of tonsils or lymph glands. Blood pressure 103 systolic, 80 dias-
tolic. Examination otherwise negative.

Treatment: — This was the first patient for the proposed treatment, and she was
qloser to coma than was desired for a first trial. Accordingly the attempt was
made to be conservative. She was put to bed and a light supper ordered of two
eggs, a slice of toast, and a cup of milk-cocoa. Breakfast the next morning in-
cluded oatmeal; the rest of the diet was light and included vegetables and potato
in limited quantities. Notice should be taken that the blank food space in the
graphic chart for Feb. 24 to 25 does not represent fasting, but exact reckoning
of the diet was impossible because cooking and other arrangements were not in
readiness. At the same time liquids were forced to 6 or 7 liters per day, and alkali
was given as stated under acidosis below. As coma was imminent, there was no
choice but to take the chance of beginning the proposed treatment. Therefore
Feb. 27 was a vegetable day with 45 gm. carbohydrate and 530 calories. Feb. 28
was a fast-day with nothing but 200 calories of whisky. Marked improvement was
evident in the urine, which became alkaline, but there was a large bicarbonate
edema as illustrated by the weight curve, and weakness and drowsiness con-
tinued. Then, in order to guard against any supposed dangers of fasting, 20 gm.
oatmeal were permitted on Mar. 1, increased to 52.5 gm. on Mar. 2. By this
time glycosuria and coma symptoms were entirely cleared up, and alkali was di-
minished. On Mar. 3 the diet consisted of soy beans and green vegetables. On
Mar. 4 the diet was greatly reduced, consisting only of 90 gm. banana, 20 gm. oat-
meal, 10 gm. potato, and 10 gm. cream. The patient was extremely weak, there-
fore the attempt was made to build her up by a routine diabetic diet, in the hope
that she might be strengthened for later undernutrition treatment. No gain of
weight or strength was achieved, but glycosuria returned and the persisting acido-
sis was greatly increased, as shown in the graphic record. It was again reduced
by undernutrition, and brought to a minimum by a fast-day on Mar. 23. A
carbohydrate period was then instituted to clear up the tendency to acidosis if
possible, and the opportunity was taken to compare the assimilation of oatmeal

CASE RECORDS 179

and pure starch. On Mar. 24, 40 gm. Kahlbaum's soluble starch were the only
nourishment given, and 80 gm. on each of the succeeding days, in ten doses of 8
gm. each. On Mar. 29 a change was made to oatmeal, reducing the quantity of
carbohydrate slightly as an allowance for the oat protein. Nevertheless a gly-
cosuria of 1.39 gm. appeared on Mar. 31, proving the absence of any superiority
of assimilation of the oatmeal over the soluble starch. The resulting traces of
glycosuria were cleared up by a fast -day on Apr. 1 . Acidosis now being entirely
absent, another attempt was made to overcome the persistent weakness by as
high a diet as possible without glycosuria. Though the attempt was made to
balance protein, fat, and carbohydrate to this end, the graphic record shows that
acidosis returned promptly, and glycosuria resulted on Apr. 12. This was cleared
up by a fast-day on Apr. 14. The attempt was then made to build up strength by
still higher diet and to diminish acidosis by increasing carbohydrate, even at the
cost of glycosuria, with the idea that glycosuria could later be checked by brief
fasting. Acidosis was not controlled, and weight and strength were not gained,
and on Apr. 25 this attempt was abandoned. From this date to May 1, pure pro-
teici-fat diet was attempted, but both glycosuria and acidosis were present. At
this time a more rigid program of undernutrition was begun. It will be seen
chat the calories during May averaged less than 1000 daily, a maximum of car-
bohydrate was introduced, and frequent fast-days were employed. The weight
diminished very slightly. The complaints of weakness were about the same.
Most of this period from May 1 to the end of July was vegetarian, chiefly nuts
and green vegetables, of which the patient was fond. On June 30 an enormous fat
intake was permitted experimentally, as mentioned under acidosis. No special
virtue of the vegetarian regime was perceptible. Glycosuria and acidosis were
practically absent during the undernutrition of the month of May; both returned
with the higher caloric diet of June and July. This period was terminated be-
cause of the increasing weakness of the patient, due particularly to the low pro-
tein. In the period July 10 to 14 a test was made with raw pancreas feeding as
described in Chapter IV.

Most of the month of Aug. was occupied with pure protein-fat diet of between
1000 and 1100 calories, and about 30 gm. protein. The patient was relieved
of the fast-days, of which she had been complaining bitterly. Glycosuria was
mostly absent, but acidosis was persistent. In Sept. the calories were increased,
partly by use of alcohol, and a few fast-days mitigated by vegetables or alcohol
were employed. Weight and strength were not thereby improved, and both
glycosuria and acidosis were troublesome. Oct. was a period of marked undernu-
trition, the calories being mostly about 900 daily, carbohydrate-free, except for
two tests in which respectively 60 and 58. 8 gm. carbohydrate resulted in glycosuria,
when added to this caloric intake. In Nov. and Dec. the carbohydrate-free diet
was pushed to the upper limit of tolerance, so that traces of glycosuria and keto-
nuria kept recurring and were checked by occasional fast-days. The attempt
thus to build up weight and strength failed as usual. The patient was dismissed

180 CHAPTER m

on Dec. 20 with instructions to continue diet as during Dec. and to take a fast-
day once each week.

Acidosis. — ^The excretion of acetone bodies in the first few days was evidently
very high, but the analyses were lost. Notwithstanding the alkali dosage, the
urine was strongly acid, and the ammonia nitrogen was 1.7 gm. on Feb. 25 and
1.93 gm. on Feb. 26. Each day the patient took 2.4 gm. potassium citrate, small
quantities of light magnesia, and calcium carbonate in quantities equal to the so-
diurii bicarbonate. It was thus hoped to provide a balance of salts, and perhaps
also to neutralize some acid with a non-irritating substance such as chalk. The
sodium bicarbonate dosage was as follows: Feb. 25, 20 gm.; Feb. 26, 32 gm.; Feb.
27, 72 gm.; Feb. 28, 48 gm.; Mar. 1 to 7, 40 gm. daily; Mar. 8 to 20, 20 gm. daily.
All alkali was stopped at this time. No efiect upon the carbohydrate tolerance
was evident.

As mentioned, acidosis was brought under control by the initial undernutri-
tion period. With the high diets (Mar. 10 to 15) it returned very markedly, the
ammonia nitrogen rising slightly above 1 gm. notwithstanding the alkali dosage,
and the ketonuria reaching 28.7 gm. (as j8-oxybutyric) on Mar. 15. With a single
fast-day (Mar. 16) the ammonia nitrogen fell to 0.63 gm. and the acetone bodies
to 9.57 gm. With reduced diet the acidosis diminished further, and, was entirely
abolished by the carbohydrate period, Mar. 24 to 31, the ammonia and acetone
figures falling to normal, and the ferric chloride reaction turning entirely negative.
MildCT acidosis returned with the beginning of mixed diet after Apr. 2, and it was
proved that carbohydrate, even to the point of causing glycosuria, could not keep
acidosis absent. Especially in the period Apr. 19 to 24 the carbohydrate was
gradually increased to 90 gm., with a total diet as high as 2800 calories (over 75
calories per kg. on 37 kg. weight). The highest glycosuria resulting was 7.26
gm. on Apr. 24. This program was adopted on the principle frequently stated
in the literature, that 90 gm. carbohydrate intake is worth a glycosuria of 7 gm.
The attempt was to build up weight and strength with the high diet, while keep-
ing acidosis in check by a favorable carbohydrate balance. Acidosis, however,
remained present as stated, and the peculiar weakness and malaise characteristic
of severely diabetic patients with even moderate acidosis persisted likewise.
Carbohydrate had to be discontinued in order to check the steady increase of gly-
cosuria. Thus the diets of Apr. 29 to 30 consisted of 61 gm. protein and 200 gm.
fat. Both protein and fat were then diminished, until on May 1 the diet was 53
gm. protein and 177 gm. fat. This would correspond to an orthodox diabetic diet
of about 1.5 gm. protein and 37 calories per kg. Nevertheless slight glycosuria
and heavy ferric chloride reactions persisted, and the ammonia nitrogen by May
1 was up to 1.2 gm. May 2 was a fast-day with 34 gm. butter, this quantity of
fat being abnost negligible for either good or ill. The glycosuria ceased before the
close of the 24 hours, the ferric chloride reaction diminished to a trace, and the
ammonia nitrogen fell to 0.6 gm. Thus 1 day of undernutrition accomplished
' what had been impossible on full diets either rich or poor in carbohydrate.

CASE RECORDS

181

For the next 3 months a vegetarian r6gime was tried, as described under "weight
and nutrition" below. Because of the low protein and fat, a relatively high car-
bohydrate tolerance was exhibited, which was also assisted by the very frequent
fast-days. In this way both glycosuria and acidosis were almost continuously
absent for a month. The hope of a gain in tolerance was disappointed, however,
as demonstrated by the prompt return of both glycosuria and ketonuria when a
moderate increase of diet was attempted in June and July.

On June 30 an enormous fat intake was allowed experimentally for a single
day, followed by a series of lower diets, as shown in Table II.

TABLE n.

Diet.

Urine.

Date.

Protein.

Fat.

Carbo-
hydrate.

Calories.

Volume.

Sugar.

Total
nitrogen.

NH.-N

Acetone

bodies (as

l8-oxy-

butyric).

IHM

gm-

gm.

im.

cc.

gm.

gm.

gm.

gm.

June 27

43.1

104.7

87.0

1403

2320

+

4.02

0.35

0.78

" 28

40.0

104.8

85.9

1415

3188

3.31

4.38

0.41

1.66

" 29

0.5

123.9

3.4

1270*

1858

0

2.17

0.35

0.62

" 30

83.6

448.6

72.4

4456

2128

+

4.55

0.92

4.67

July 1

74.7

292.8

51.0

2707

2629

4.12

11.38

1.34

8.57

" 2

57.4

185.7

64.0

2013

1422

7.11

4.54

0.91

3.21

« 3

57.6

202.0

68.3

2107

1852

14.63

6.22

2.00

5.64

" 4

41.0

112.0

39.0

1295

1411

4.06

6.28

1.50

. 2.73

" S

0.2

0.2

1.8

290t

1506

0

4.14

0.80

0.47

" 6

36.3

109.8

72.6

1315

1528

0

6.17

0.38

1.11

" 7

55.1

101.2

68.2

1420

1630

0

7.02

0.43

0.48

* Butter 150 gm., strawberties 50 gm., alcohol 25 gm.
t Alcohol 40 gm.

The relation between combustion of food fat and body fat is here illustrated.
The huge ration of June 30 did not produce any explosive increase of acidosis. The
acetone bodies showed a rise on the same day, but a more marked one the follow-
ing day, while the ammonia nitrogen did not reach its summit until July 3. It is
evident that what happened was not the conversion of any large proportion of the
fat on June 30 into acetone bodies, but rather an injury of fat assimilation pro-
duced by this excess and continued by reason of the fat rations (lower but still
excessive) of July 1 to 3. On the fast-day of July 5, storage or depot fat was
necessarily burned, yet the ammonia nitrogen was approximately the same as On
June 30. On July 6, with a limited fat intake, the effect of carbohydrate was
evident in producing a lower ammonia nitrogen excretion than on the fast-day.
The entire observation is against the idea of a difference between food fat and

182 CHAPTER in

body fat in combustion, and indicates rather an overtaxing of fat metabolism by
excessive intake and improvement of assimilation by relief from the strain.

On the carbohydrate-free diet beginning in Aug., strong ferric chloride reactions
and unduly high ammonia excretion were the rule. Temporary control of both
glycosuria and acidosis was achieved with the low diets (about 900 calories) in early
Oct. Thereafter it will be noted that the ferric chloride reactions were some-
times negative and never more than slight, even on carbohydrate-free diet, the gen-
eral diabetic condition being now under better control. The continuance of slight
acidosis, however, throughout so much of the period of treatment represents one
of the serious mistakes in the management of this case.

Weight and Nutrition. — ^Weight at admission 40.1 kg., at discharge 35.2 kg.;
i.e., a loss of 4.9 kg. The initial gain in weight, up to 43.5 kg. on Feb. 28, repre-
sented a marked bicarbonate edema, simultaneous with the turning alkahne of
the urine. Slighter edema was present on certain occasions later, notably Aug.
15 and Nov. 7, being due apparently to sodium chloride and removed by diminish-
ing the salt intake.

On Mar. 21 the large fluid intake began to be restricted. The patient had
been accustomed to large quantities of water for some months past and com-
plained of thirst when the allowance was diminished by order; within a few days
this complaint disappeared and the thirst remained normal thereafter.

Vegetarian diet was tried for a period of nearly 3 months, chiefly because of
the claims in some quarters concerning differences in the glycosuric effect of
different proteins, and the bare possibility that meat protein might at least
stimulate a greater flow of gastric juice and correspondingly of pancreatic juice,
and thus perhaps depress the internal function of the pancreas by stimulating
its external function. Undernutrition was employed at the same time to create
the most favorable conditions, and acidosis was kept absent by such quantities
of carbohydrate as seemed within the tolerance. Butter was regularly allowed,
eggs rather frequently, and a Uttle bacon and bacon fat sometimes, but for much
of the time the ration was vegetarian in the strictest sense, composed entirely of
vegetables, fruits, nuts, soy beans, and occasional gluten preparations. There
was no gain of tolerance, and no advantages of a vegetarian diet or evidence of
specific differences between proteins were observed.

Neither food nor feces was analyzed. The former was calculated as usual
from the Atwater-Benedict tables. On this basis the following reckoning can be
made for the period from Mar. 16 to Nov. 30, for which the records of both food
and urine are complete. Also, the total period of 260 days is divisible into two
nearly equal portions, namely, 136 days up to July 31, during which the diet was
largely and sometimes wholly vegetarian and contained considerable carbo-
hydrate, and 124 days after July 31, in which the protein was of animal origin
and the diet was almost continuously carbohydrate-free. The results for the
various periods may be compared as shown in Table III.

CASE RECORDS

183

^

ej .

g (^ 10 irj

3 !3

S CN ■^ll 0

o5

fe^ T-J 0\ ro

.■§ o

a g

gm.
2.63
0.21
2.40

H

T-4 0 ^

1 (M S .rt

_g

i^ 0\ 00

■3 fl 2

0\ O; o\

■SS-S

S 0;' CO d

Hss

5 0 10 ^H

^ o\ t>»

■3

i-H

Total
nitrogen

in diet
per day
per kg.

0. c^ vo

E d d d

2* fl-.. t^

. ■* ^ lO

g CN >0 0

"^ t^ 00 \o

A .S

nitr
n in
prote
5.25).

0 CN ■*
S IN 0\' «

" S^.i.

Si cio in CN

00 o_ 00

0 aj '

H ■■V

w ^

M

Average
protein
per day
per kg.

sm.
1.23
1.44
1.02

a

!•§&■

. <N rf OS

tH^TJ

E "3 ro t^'

f^

I^R

h3

Th 10 re

g

2

•<l; 0 f)

H

3'a*.-

.000

o'S.S

S « tN rC

H^-o

^ *^ ^., ^

g

^" vo" i^

a

-'

Average
calories
per kg.

per day.

ce ro re

CO PO re

t|l

ro ■* T-i

^ 0 !N

C>l^ CN_ CN

.5

<N SO vo

si^"

*^ to w

Ce_ (N VH

,|,

•W as 0" ■

^ -"^ so
CO « ^

en

>,

tS

-a

^ 1

0 "5 "C

so 0 OJ

IN -a a

^ ^=«

• 2 n •— 4

tal per
nimal'
egetab

£<>

H

::

;;

1

184 CHAPTER ni

The patient lost 5 kg. weight in 9 months. If it be assumed that 90 per cent
of a weight change is ascribable to fat, in this instance the loss of nitrogenous
"tissue" would not exceed 500 gm. Using Voit's figure of 3.4 per cent N, the
possible loss of body nitrogen would then be 17 gm. If it be urged that in an
emaciated person the wasting of "tissue" in proportion to fat is higher, the
above comparison of intake and output shows that the patient must have been
nearly in equilibrium. At worst, the nitrogen deficit must have been small, and
it may be assumed that the diet fulfilled the purpose of protecting body protein
from any extreme loss while maintaining prolonged undernutrition.

Two deductions seem justified. (1) Digestion and absorption of protein
were, as would be expected, distinctly better during the "animal" period, but the
utilization of vegetable proteins, including the times when the diet was exclu-
sively vegetable, was reasonably satisfactory. (2) Though the nitrogen intake
was lower in the "vegetable" period, it must be called low also in the "animal"
period, and it is evident that there is no serious obstacle to maintaining equilib-
rium on strict carbohydrate-free diet with a low protein ration. It is to be borne
in mind that the energy intake is a question not of food ingested but of food ab-
sorbed. If it be permissible to assume that the same proportion of total calories
as of nitrogen was lost in the feces, viz. 11.29 per cent, subtraction of this num-
ber from the 33 calories ingested daily would leave an average of between 29 and
30 calories absorbed daily per kg. of body weight. Accordingly, it would appear
that this patient lived for 260 days on an average of 0.173 gm. N and 30 calories
per kg. Work and exposure to cold were both far less than in ordinary individuals.
On the other hand, the rather tall, very emaciated figure presented a dispropor-
tionate surface. Losses in sugar and acetone bodies were sKght. On the whole,
the figures obtained correspond satisfactorily to the known laws of metabolism
in normal persons.

Subsequent History. — On Jan. 14, 1915, the patient reported by telephone that
she was feeling well and had cleared up occasional traces of glycosuria by fast-
days. On Jan. 20 she reported increasing difficulty in remaining sugar-free, and
was instructed to return to the hospital if difficulty continued. Nothing more
was heard until Apr. 1, when a letter stated that she had returned to her home
in Indiana. On Apr. 26 a response to a letter of inquiry showed that the cause of
her silence and removal was her adoption of Christian Science. Occasional
later reports showed that she was eating everything at will, including much
candy,, and gradually losing strength. Death occurred from simple weakness
the first of Oct. 1915, the terminal collapse being brought on by taking a dose of
Epsom salts.

Remarks. — The patient, when received, was undoubtedly close to coma. She
appeared then as having diabetes of extreme severity. The results obtained
seemed highly favorable. In the light of later experience this treatment was
very bad.

Part of the fault lay with the patient, who had always eaten injudiciously

CASE RECORDS 185

and was the most unruly of the entire series for dietary control. The high
diets, the persistence of glycosuria and ketonuria through considerable periods,
and the changes in program from time to time were in some measure forced by the
necessity of appeasing the patient's demands and meeting her psychic needs.
She insisted not only upon nourishment but also taste and satiety, and slight pri-
vations brought on hysterical tears and melancholy which seemed serious as a
possible influence upon the diabetes, though, as a matter of fact, no particular
influence of psychic upsets upon the food tolerance was observed. She was given
unusual leeway as being the first patient.

The cause of the final disaster was also instructive. It is noteworthy that al-
though a very careful limitation of diet both quantitatively and qualitatively
had resulted in threatened coma at the time of admission, subsequently on abso-
lutely unrestricted diet no symptoms of acidosis were described, evidently be-
cause the patient lived so largely on carbohydrate, and the polyiiria aided in the
elimination of acetone bodies. Although the patient was young and the kind
that typically dies in coma, death occurred from simple wasting and asthenia.

The chief difficulty consisted in inexperience with the treatment. The cautious
manner of beginning treatment, and the partial, irregular, and inadequate charac-
ter of the measures employed belonged to this stage of uncertainty and orienta-
tion. It showed the viciousness of some of the accepted methods in the man-
agement of diabetes. The same patient admitted at a later time could have been
treated far better; and the case, though severe, was mild in comparison with
some of the later ones. A bold initial fast, followed by testing of the tolerance
for different classes of food and arrangement of a diet accordingly, would have
brought far quicker and better results.

The actual accomplishment was that the patient was kept alive in the hospital
from Feb. 24 to Dec. 20, with a loss of 5 kg. (one-eighth of her weight at en-
trance), and about a corresponding diminution of strength. Glycosuria and
acidosis were kept entirely absent at certain times, and were controlled within
small quantities at all times. Actual food tolerance was slightly less at the end
than in the earlier part of treatment, and the progress was slowly but distinctly
downward. The bungling and inadequate treatment furnished abundant reason
for this slight downward progress in 10 months, and no "spontaneous" cause
need be assumed. Methods and results of this sort have been common with a
large proportion of practitioners who have undertaken to apply the fasting
therapy. The record of this patient stands as a useful example of how a case
should not be treated.

CASE NO. 2.

Female, unmarried, age 17 yrs. Italian, sewing machine operator. Ad-
mitted Apr. 13, 1914.

Family History. — Grandparents healthy as far as known. Father a day laborer
and short of stature; weight about 200 pounds. Mother short, normal figure,

CASE RECORDS 187

was agreeable to this Italian patient. In other words, the fast was not broken
(as usual) by carbohydrate alone, but fat was introduced to make a total of 2000
calories. Also on the following days, diets low and relatively high in fat were
comparfed, and on Apr. 30 a day of 100 gm. olive oil was given instead of a regu-
lar fast-day, according to the practice of some authorities. The results are dis-
cussed elsewhere (Chapter VI). They illustrate the harmfulness of attempts to
use fat in this manner. In the first few days of May a rather low diet was given,
with absence of glycosuria. The succeeding period represents a low calory diet,
with as much carbohydrate as possible and frequently repeated fast-days for the
purpose of overcoming the persistent ferric chloride reaction. On June 11 an
enormous fat diet was given (137 gm. protein, 34 gm. carbohydrate, 6672 calories
= 167 calories per kg.) . A slight rise in the ammonia followed, but the patient's
appetite was spoiled so she could take only a low diet for several days. On June
17 a less extreme fat diet was begun, which nevertheless represented not far from
100 calories per kg. of body weight. The results are discussed in Chapter VI.
The onset of glycosuria and the marked rise of acidosis are the striking features.
July S was a fast-day with alcohol. Thereafter a low diet was given, relatively
rich in carbohydrate. Under this program both glycosuria and acidosis cleared
up and were kept absent.

The patient was discharged Aug. 14, symptom-free and feeling well and strong.
The hospital stay was uneventful except for occasional headaches for which no
cause was found.

Acidosis. — Although there were no signs of coma, the analyses in the first few
days indicated that trouble would have resulted before long on the restricted
diet. On Apr. 14 to IS no alkali was given, and the urine contained 2.4 to 2.7
gm. ammonia nitrogen and 4.2 to 7.0 gm. acetone bodies (as |S-oxybutyric) .
Apr. 16 to 20, 20 gm. sodium bicarbonate were given daily, and 10 gm. on Apr. 21,
after which alkali was stopped. The rise of ketonuria, up to 12.1 gm. /3-oxybutyric
acid on Apr. 18, was to be expected, but at the same time the ammonia, instead of
falling, remained little changed, and actually rose to 3.1 gm. ammonia nitrogen
on Apr. 18. With diminished fat and increased carbohydrate intake on Apr. 19
there was a drop in both ammonia and total nitrogen, but the steepest fall of the
ammonia occurred on fasting. Thereafter the three principal peaks of the
ammonia curve (Apr. 23, May 2, and June 19 to July 3) are clearly associated
with the fat content of the diet. It is evident from the graphic chart that acidosis
was not checked by hberal quantities of carbohydrate and protein, nor by a fav-
orable carbohydrate balance, but on the contrary rose and fell according to the
ingestion of fat. For about the last month in the hospital acidosis was entirely
absent on a diet moderate in protein, relatively abundant in carbohydrate, and
low in fat.

Weight and Nutrition. — Weight at admission 42.6 kg., at discharge 40 kg.;
i,e., a loss of 2.6 kg. The variations and excesses in diet were experimental.
The diet at discharge was approximately 56 gm. protein, 120 gm. carbohydrate.

188 CHAPTER in

and 1400 calories (1.4 gm. protein and 35 calories per kg., reduced slightly by
occasional fast-days). The patient's figure and strength at discharge appeared
normal. The diet was planned as one on which she could work. She was in-
structed not to gain weight, and it was proposed to give her instructions there-
after chiefly on the basis of her body weight.

Remarks. — ^Aside from the intentional experimental variations, the treatment
was fairly efficient and the result good. The reduction in weight and the arrange-
ment of the final diet, restricted in total calories, adequate "in protein and rather
liberal in carbohydrate, was about what was needed for a relatively mild case,
such as this one by this time had proved itself to be. By comparison of the
diets of Apr. 14, IS, 18, and 19 with those of Aug. 9 and 11, it will be seen that
the calories are about the same, while the carbohydrate, counting also that deriva-
ble from proteia, is higher in the latter period. Along with this, the sharp
contrast as respects glycosuria and ketonuria shows a decided upward progress
in this 17 year old girl during these 4 months.

Subseqtient History. — ^After discharge on Aug. 14, the patient followed diet and
remained sugar-free for about a month at home. Owing to poverty it was almost
impossible for her to obtain the necessary food, and she gradually began to take
the diet of the rest of the family. Sugar reappeared, followed by other symptoms.
She was readmitted Nov. 30, 1914, complaining of polydipsia, polsoiria, and for the
last few days loss of appetite and drowsiness.

Second Admission. — A 4 day fast was instituted, glycosuria ceasing on the 3rd
day. On Dec. 4, green vegetables containing 20.5 gm. carbohydrate were taken
without glycosuria. Another fast-day was then given as a therapeutic measure,
and a mixed diet of eggs, butter, steak, and vegetables gradually begun. Slight
glycosuria appeared within a few days. Beginning Dec. 16, the diet was almost
constantly carbohydrate-free and unduly high in calories. Ketonuria was pres-
ent most of the time up to July 24. Then, after a fast-day, a carbohydrate test
was given in the form of green vegetables as usual. Beginning with 10 gm. car-
bohydrate on July 26, an increase of 10 gm. daily was made. Aug. 4, on 100 gm.
carbohydrate, she showed a trace of sugar, which disappeared the next day when
the same carbohydrate was given. The true hmit was reached on Aug. 8 with
130 gm. carbohydrate. Accordingly, 120 gm., which had been tolerated the pre-
vious day, were accepted as her tolerance. The acidosis was thus cleared up
(compare with increase of acidosis when fat was given in Apr., 1914). It returned
in smaU amount on the subsequent carbohydrate-free diet, then diminished, so
that after Sept. 7 it was absent. Another carbohydrate tolerance test was madfe
beginning Oct. 11, and the limit was found to be practically the same as in Aug.
Small quantities of carbohydrate were added to the diet in Nov., but discon-
tinued on account of glycosuria. Beginning Dec. 13, a third carbohydrate tol-
erance test showed imchanged assunilation, and cleared up the sUght ketonuria
which had again developed on protein-fat diet. Carbohydrate was again included
in a diet somewhat lower in calories, but was discontinued on account of persistent

CASE RECORDS 189

slight glycosuria. Strenuous exercise was a feature of the treatment during this
period in the hospital. The observations are discussed in Chapter V. The
patient was discharged Feb. 2, appearing healthy and well nourished and feeling
strong and capable of hard work.

Acidosis. — The ammonia excretion was constantly higher than that of normal
persons; perhaps not higher than some normal persons would show on the same
diet. No determinations were made during the carbohydrate tests, when lower
values might have been found. A fall of the ammom"a on fast-days and a rise on
carbohydrate-free diet is shown by portions of the curve in Apr., May, and June;
this is doubtless due in part to corresponding variations in total nitrogen excre-
tion, but also illustrates the difference between fasting and protein-fat diet.
Beginning Dec. S, it is evident that a fast-day, followed by a reduction of fat in
the diet while keeping protein the same, resulted in a drop in ammonia excre-
tion. The carbon dioxide-combining power of the plasma remained in the
neighborhood of normal without alkali dosage, but nevertheless showed a ten-
dency to sink somewhat below the low normal limit. This was one of the patients
who showed a fall in blood bicarbonate on fasting, as seen particularly after the
fast-days of May 1 and Sept. 12. Certain other fluctuations in this curve are dis-
cussed in Chapter V in connection with exercise.

Blood Sugar. — This was mostly about 0.2 per cent. A rise is seen at the close
of the carbohydrate tolerance test in Oct. Analyses were not made during the
other carbohydrate tests. The normal values from Apr. 30 to May 11, and on
Sept. 22 and 23, showed that a reduction was possible by suitable low calory diet,
and the failure to insist upon such a level was one of the faults of the treatment.

Weight and Nutrition. — In general the lowest diets are those of Aug. and Oct.
and the dismissal diet about the 1st of Feb. These amounted to 1300 to 1500
calories, which for a body weight of 40 kg. would equal 35 calories or more per
kg. At other times this diet was increased by fat to as much as 3500 calories,
or some 60 calories per kg. Two modifying features come into account. One
is the number of fast-days, which serve to diminish the average intake some-
what below this figure. Second, the patient was kept most of the time on very
heavy exercise, so that the caloric requirement was increased. The patient en-
tered weighing 45.6 kg.; namely, a gain of some 5 kg. since her former discharge,
with a corresponding loss of tolerance. She was dismissed weighing 39 kg.;
i.e., with a loss of 6.6 kg. in 14 months in the hospital. To this extent the treat-
ment was one of undernutrition.

Remarks. — It was above noted that during 4 months in hospital, at the first
admission, progress was upward. The patient was at home about 3i months and
broke diet in the latter portion of this period. The downward progress is plainly
evident. After her second admission she frequently showed sugar on carbohy-
drate-free diet. Also her limit of tolerance for carbohydrate alone, in the green
vegetable tests of Aug., Oct., and Dec, 1915, was almost exactly the quantity
which could be included in her regular mixed diet in Aug., 1914, without any

190 CHAPTER III

appearance of glycosuria. It is thus clearly confirmed that a marked and last-
ing injury of assimilation can be produced by a few months of unregulated diet.
On the other hand, the former carbohydrate tolerance tests of Aug., Oct., and
Dec, 1915, covered a period of S months, and conclusively proved the absence of
any perceptible downward progress during that time. Also the weight remained
essentially the same, so that no disturbing factor was thus introduced. Moreover,
comparison of the tolerance at the beginning and end of the second hospital
period shows that glycosuria appeared on Dec. 14, 1914, on a diet of 60 gm. pro-
tein, 42 gm. carbohydrate, and 981 calories. If all these earlier occurrences of
slight glycosuria be ignored, it is still evident that on repeated occasions in Jan.,
Feb., and thereafter, glycosuria was present on carbohydrate-free diets of some
1700 calories. In contrast to this, it is seen that from Dec. 27, 1915, to Jan. 1,
1916, a diet of 1760 calories with 10 to 30 gm. carbohydrate was tolerated without
glycosuria, and the protein in this diet was fully as high as in the above men-
tioned carbohydrate-free periods. Glycosuria appeared only on Jan. 6, toward
the close of another week on the 30 gm. carbohydrate allowance. It was thus
present on Jan. 11, but cleared up on withdrawing carbohydrate from the diet.
A slight gain in food tolerance is thus evident during these 14 months in hospital,
and this upward tendency is the more remarkable in view of the improper treat-
ment, with its long periods of overfeeding and almost continuous marked hyper-
glycemia. The essential criticism of the treatment in this period is that by
pernicious protein-fat overfeeding (up to 60 calories per kg.) it held back the ten-
dency to improvement, and ultimately sacrificed 6| kg. weight for only the slight
gain of assimilation above mentioned. An excellent physical condition was main-
tained throughout, and the patient was discharged seemingly in splendid health.
The failure of the plan of feeding for immediate weight and strength is well dem-
onstrated by this prolonged trial. The transitory well-being is too dearly bought
at the price indicated by the laboratory findings. Proper management would
have imposed a rigid low diet from the outset and insisted upon continuously
normal urine and blood. A sharper initial fall of weight would have resulted.
A small quantity of carbohydrate could have been included in such a low calory
diet. Under such a program there is little doubt that the patient could have been
discharged in fully as good physical condition and on fully as high a total diet as
was actually the case; and the diet could have been balanced properly with car-
bohydrate, and the entire condition from the standpoint of the diabetes would
have been far more favorable.

Subsequent History. — After discharge on Feb. 2, 1916, diet was followed until
Mar. 8, when the patient began to take two slices of bread daily in addition to the
weighed diet, because of a strong craving for carbohydrate. Sugar had been ab-
sent before, but then reappeared and continued. She was doing 5 hours work
on the sewing machine at home and 2 hours housework daily, and in addition
walked two miles two or three times a week. A fast-day was taken once a week
up to the 1st of Mar.

CASE RECORDS 191

Third Admission. — Mar. 20, 1916. Weight 39.4 kg. Nutrition and strength
still appeared very good. Fasting was imposed Mar. 21 to 23 inclusive, then low
protein-fat diet, gradually increasing from 1000 to 1200 up to 1800 calories, with
protein ranging from 40 or 50 up to 60 or 70 gm. daily. The patient was again
discharged on July 12 at her own request, still appearing in excellent condition.
Headaches had been somewhat relieved after prescription of glasses by an
oculist.

Acidosis. — It is of interest that heavy acidosis was brought on by the addition
of two slices of bread to the weighed diet on which both glycosuria and acidosis
had been absent. Fasting was begun on the day following admission (Mar. 21).
The patient was depressed, dizzy, and significantly unwell. The finding of 33.4
per cent plasma bicarbonate showed the reason. Sodium bicarbonate was then
given in 3 doses of 10 gm. each. Within half an hour after the first dose the clini
cal effect was striking. The headache, dizziness, depression, and malaise van-
ished, and were replaced by comfort and cheerfulness. It is possible that fasting
alone would have been badly borne, as the tendency to a fall in blood alkalinity
on fasting was previously noted in this patient. No more alkali was given. The
CO2 capacity was found normal on the day after the bicarbonate dosage, but fell
to 46 per cent on the succeeding day (Mar. 23). On this day also glycosuria
ceased. Mar. 24 to 27, a trial was made of carbohydrate-free diet, which fre-
quently relieves fasting acidosis. On Mar. 24 nothing but 21 gm. protein was
fed, the diet being coffee, soup, and veal. The blood bicarbonate rose a trifle.
On Mar. 25 the diet contained 40 gm. protein and 800 calories. Thereafter pro-
tein was increased and fat diminished, so that on Mar. 27 the diet was 70 gm.
protein and 600 calories. The net result of these low protein-fat rations was
that by the morning of Mar. 26 the blood bicarbonate had risen to 52.8 per cent.
On Mar. 28, the diet was sharply reduced to 16 gm. protein and 10 gm. carbohy-
drate. The blood alkalinity fell sharply as on a fast-day; i.e., to 40 per cent on the
morning of Mar. 29. Beginning Mar. 29, the diet was limited to green vegetables.
On this, by the morning of Mar. 31, the CO2 capacity had risen to 44 per cent,
though the carbohydrate intake had amounted to only 30 gm. on Mar. 30. By
Apr. 7, the plasma alkalinity had risen to within normal limits on low protein-fat
diet. Thereafter it remained generally at a low normal level. No reason is
known for the low reading of 45.6 per cent on June 27, unless it were the in-
creased fat intake. By July 7, it had returned to normal without the aid of
alkali, possibly with the aid of the small allowance of carbohydrate. The other
tests were not parallel with the plasma bicarbonate. The ammonia nitrogen
at first fell from 3.4 gm. on Mar. 20 to 1.94 gm. on Mar. 22, then remained nearly
stationary to Mar. 27, thus corresponding to the plasma bicarbonate. But
when the plasma bicarbonate fell at the beginning of the vegetable period, the
ammonia fell also. Later, on protein-fat diet, the ammonia was a more sensitive
indicator of acidosis than the plasma bicarbonate, being unduly high (Apr. 14,
June 6 to 8) at times when the plasma bicarbonate was approximately normal.

192 CHAPTER m

The ferric chloride reaction became negative early in the vegetable period, at
the very time when the plasma bicarbonate fell. It remained negative thereafter.

Blood Sugar. — ^The fall during the initial period of fasting and undernutrition
is evident from the graphic record. Subsequently it rose, and remained much
of the time in the neighborhood of 0.2 per cent. The decline to a nearly nor-
mal value shortly before discharge is in conformity with the other improvement.

Weight and Nutrition.— Weight at admission 39.3 kg.; i.e., the same as at the
previous discharge. Weight at discharge 35.2 kg. Nearly 4 months of treat-
ment thus represented undernutrition to the extent of 4.1 kg. This under-
nutrition was imposed especially at the beginning of this hospital period. -From
Apr. 18 to discharge there was an actual gain of 1 kg. During most of the time
one egg was allowed on fast-days, but beginning with July the fast-days were
made absolute. The daily allowance of 70 gm. protein, 10 to 15 gm. carbohydrate,
and 1800 calories was thus reduced to an average of 60 gm. protein and 1540
calories (1.7 gm. protein and 44 calories per kg.).

Remarks. — The carbohydrate tolerance test Mar. 28 to Apr. 4 showed an assimi-
lation not above 60 gm. carbohydrate. Glycosuria also appeared subsequently on
protein-fat diets lower than those previously tolerated. Very decided downward
progress was thus clearly demonstrated in consequence of violations of diet,
during less than 2 months at home, the violations being said to have been limited
to less than 1 month. Susceptibihty of this case to rapid downward progress
on dietary overstrain is thus proved. On the other hand, in nearly 4 months
of hospital sojourn this time, the progress was demonstrably upward. From
Apr. 18 onward, as mentioned, there was a gain of 1 kg. weight, and at the same
time the patient became able to remain free from glycosuria and ketonuria on
diets decidedly higher in protein, fat, and carbohydrate than those on which
glycosuria repeatedly occurred earUer in the period. The tendency of the blood
sugar likewise was downward. Furthermore this improvement occurred in spite
of grossly excessive diets, the tendency to spontaneous upward progress being
thus all the more remarkable. In extenuation of the diet only two excuses can
be offered. One is that the patient was taking heavy exercise, and it had not
yet been learned that this does not atone for excessive diet. The other is that
it was known that the patient at home would not adhere to any diet which kept
her at all hungry or uncomfortable. Accordingly she was allowed this diet, on
which her progress seemed at least temporarily favorable, in preference to a
more beneficial diet which would be more Uable to be violated.

Fourth Admission. — Sept. 11, 1916. (No graphic chart.) Patient returned to
hospital with the usual history of having broken diet. Heavy sugar and ferric
chloride reactions were now present on her former diet. A 4 day fast was neces-
sary. A carbohydrate test with green vegetables in the usual manner showed a
tolerance of 50 gm. A carbohydrate-free diet was then begun, with 40 gm. pro-
tein and 600 calories. The experiment was then performed of keeping this pro-
tern the same while gradually increasing fat to make a totalof 1300 calories (see

CASE ItECOEDS 193

Chapter VI). The result was glycosuria, while the ferric chloride reaction re-
mained negative. Thereafter with less fat (900 to 1200 total calories) and the
same protein, glycosuria was absent, but returned when the protein was in-
creased to SO to 65 gm. She was discharged on Dec. 4, 1916, stiU in fair subjective
health.

Acidosis. — The COj capacity of the plasma at first was 35.5 per cent. Weak-
ness and malaise, making her imfit for work, were the only clinical symptoms of
acidosis. With 4 days of fasting, the CO2 capacity rose to 53.3 per cent. After 2
days respectively of 10 and 20 gm. carbohydrate, it was 59.5 per cent, and at the
close of the carbohydrate test (Sept. 22) 58 per cent. This reaction to fasting is
noteworthy ia a patient who on previous admissions had shown such decided
falls in blood bicarbonate on fasting. Likewise the heavy ferric chloride reaction
diminished on fasting and cleared up during the vegetable period. The am-
monia nitrogen, which was 3.3 gm. on the prescribed diet, dropped to 2 gm.
at the close of fasting, and to 0.43 gm. on the fast-day (Sept. 23) following the
vegetable period. Thereafter on protein-fat diets the plasma bicarbonate re-
mained at a high normal level (59.8 to 68.8 per cent) and the ferric chloride reac-
tion continued negative. The ammonia nitrogen ranged from 0.8 to 1.5 gm.,
and was thus the most delicate index of acidosis.

Blood Sugar. — This was 0.218 per cent in whole blood and 0.238 per cent in
plasma on the first day of fasting (Sept. 13), 0.192 per cent in plasma on the last
day of fasting (Sept. 16). It was never brought lower than 0.122 per cent in
whole blood and 0.147 per cent in plasma. The last analysis, with sugar-free
urine, showed 0.202 per cent plasma sugar.

Weight and Nutrition. — ^Weight at admission 41 kg., part of which was edema.
Weight at discharge 34.3 kg. The final weight was thus only about 1 kg. less
than at the previous discharge, but otherwise the condition was much worse.
The carbohydrate test above mentioned indicated a loss of only 10 gm. tolerance.
A truer index is afforded by the fact that traces of glycosuria now tended to ap-
pear on relatively low carbohydrate-free diet. In contrast to the 70 gm. protein,
10 to 15 gm. carbohydrate, and 1800 calories tolerated at the former discharge,
the diet at discharge this time had to be limited to 45 gm. protein and 1200 calories
(1.3 gm. protein and 35 calories per kg., reduced by the weekly fast-days to 1.1
gm. protein and 30 calories average). Moreover, marked hyperglycemia was con-
tinuous on this diet as stated, and glycosuria appeared upon very slight increase
of either protein or fat. The patient had again demonstrated how rapidly she
could progress downward with improper diet in the short period of 2 months at
home. At this discharge she was distinctly weaker than ever before, though still
comfortable and able to do housework. The treatment had not been radical, but
she had been fed during the whole of this hospital period to the limit of her
tolerance in order to keep up her weight and strength.

Subsequent History. — A note received from the family Mar. 14, 1917, stated that
the patient died at 2:30 a.m. that day. She had again broken diet because of the

194 CHAPTER III

unfavorable environment, and the diabetes took its natural rapid course. She
refused the petitions of her family that she return to the hospital.

Remarks. — ^The patient had been kept alive and almost uninterruptedly com-
fortable for 3 years under treatment. In view of her state of intelligence, will
power, and environment, this was probably as much as could have been accom-
plished unless she had been kept continuously in an institution. The chief
scientific interest in the case lies in its demonstration of rapid downward progress
with dietary indiscretions, and complete absence of downward progress and
distinct tendency to upward progress even under treatment which never was
radical enough to remove the continuous evidences of slight metabolic overstrain.

CASE NO. 3.

.Female, unmarried, age 26 yrs. American; no occupation. Admitted May
23, 1914.

Family History. — Father was never strong, and died when patient was 5 years
old. Autopsy is said to have revealed numerous intestinal ulcers. His parents
lived to healthy old age. Patient's mother is alive and well; her father died at age
of 28 of tuberculosis said to have resulted from a career of dissipation; also her
brother died of tuberculosis, and her sister with acute melancholia. Patient
has one brother aged 32 who suffers from nervousness and indigestion. No
diabetes or other family diseases known.

; Past History. — ^Healthy life in excellent hygienic conditions, but numerous in-
fections. Measles, mumps, chicken-pox in early childhood. Typhoid at 8.
Tonsillitis at 16 with recurrent attacks in following years until right tonsil was re- '
moved 3 years ago. Only a little sore throat since then. S years ago " colitis"
for 10 days; fever, vomiting, and dull aching pain in upper abdomen, consider-
able bloody diarrhea, no jaundice. Several slight attacks of grippe, the last
about 3 years ago. 4 years ago, "intercostal rheumatism;" in bed about a
week, no herpes. Quiet life; no overstudy, but considerable social activities in
recent years, and some exhaustion after attending several dances in the same week.
Not nervous. Worry and loss of sleep for some time following unhappy love
affair 4 years ago, but this has entirely passed off. Moderate appetite, but she
has eaten even more candy than the average girl.

Present Illness.— Jan. 12, 1914, after having been in apparently perfect health,
patient woke up with malaise and slight abdominal pain. The attack subsided
with fasting and bed- rest, but on account of slight tenderness and rigidity,
laparotomy was performed on Jan. 14, revealing obliterative appendicitis and
blood clots about right ovary, treated by removal of appendix and one ovary.
Incision healed per primam, but IS days after operation phlebitis occurred, first in
left leg, then in right. Left leg has required bandaging until recently. Urine was
reported normal in hospital, but it is doubtful if tests for sugar were made.
Weakness and weariness felt at this time were attributed to convalescence and
the patient went to summer resorts to recuperate. Polyphagia, polydipsia and

CASE RECORDS

195

polyuria began, and most of her luxuriant hair fell out. The normal weight of
120 pounds diminished to 109 pounds. 2 weeks before admission, diabetes was
diagnosed. The laboratory reports showed 8.3 per cent sugar and heavy ferric
chloride reaction. A diet was prescribed containing considerable starch. Since
then, rapid dimming of vision has been noticed. Menstruation has continued.

TABLE IV.

Diet.

Urine.

Date.

Protein.

Fat.

Carbo-
hydrate.

Alcohol.

Calories.

Volume.

Sugar.

NHj-N

Acetone

3odies (as

fl-oxy-

butync).

IDM

gm.

gm.

gm.

gm.

cc.

gm.

gm.

gm.

May 24

82.8

127.5

127.7

7.5

1854

2010

47.2

1.39

2.27

" 25

126.5

175.0

272

4.0

3259

2470

68.0

1.06

2.31

" 26

:

Fast-day.

35.0

245

910

4.2

0.88

0.88

" 27

tc

25.0

175

644

0

1.00

1.63

" 28

4.2

0.8

25

—

122

825

0

1.15

1.93

" 29

10.9

2.5

60

—

302

934

0

1.23

0.64

" 30

37.0

9.5

162

—

8*8

1700

7.99

1.31

2.08

" 31

11.6

2.7

52

—

421

1362

4.22

0.34

1.05

June 1

7.0

1.2

22

—

125

1106

0

0.38

0.21

" 2

6.2

1.4

16

99

957

0

0.46

0.45

" 3

10.8

3.7

37

—

222

866

—

0.54

0.41

" 4

24.7

10.1

98

—

568

1008

0

0.53

0.37

" 5

Fast-day.

30.0

210

1758

0

0.35

0.74

" 6

14.0

1.8 1 98

—

474

774

—

0.55

0.80

" 7

Fast-day.

30.0

210

1325

0

0.32

0.35

" 8

14.0

1.7

85

—

419

727

0

0.67

0.88

" 9

31.7

6.4

144

—

779

2009

4.31

0.74

0.69

" 10

40.1

13.6

147

—

893

2278

4.57

0.43

0.48

" 11

43.7

15.1

150

—

932

2728

4.19

0.55

0.5S

" 12

1.6

—

7.8

25.0

220

2054

0

0.35

0.41

" 13

43.2

10.4

113

—

735

1969

0

0.41

0.23

" 14

40.1

11.7

124

—

778

2060

0

0.27

0.33

" 15

38.5

7.8

136

—

787

1878

0

0.26

0.31

Physical Examination. — Height 161.3 cm. Patient appears rather juvenile for
her age; stiU well nourished, and with look of perfect health. Mouth and teeth
in good condition. Right tonsil missing, left appears normal. No enlarged
lymph nodes. Reflexes normal. Examination otherwise negative.

Treatment. — (No graphic chart.) An observation diet was first permitted simi-
lar to what the patient had been taking. The initial treatment is shown in
Table IV.

196

CHAPTER in

The most disturbing symptom was the blurred vision. The patient compared
it to the efiEect of atropine. In the early days in hospital she became unable to
read even with glasses. An oculist found no organic change, and vision rap-
idly cleared in parallel with the urine. After an uneventful period of hospital
observation without return of any symptoms, the patient was discharged on
July 24.

Acidosis. — This was never heavy, and was easily controlled by reason of the
high carbohydrate tolerance. The only alkali used was 20 and IS gm. sodium
bicarbonate respectively on the &st 2 days in hospital.

Weight and Nutrition. — Weight at admission 46.5 kg., at discharge 43.4 kg.
The apparent reduction of weight was thus 3.1 kg., but actually must have been
somewhat more, as the dried tissues recovered their normal water content during
undernutrition after cessation of glycosuria. The treatment was characterized
by low protein, low calory diets, as liberal as possible in carbohydrate. At
first such diets were exclusively vegetable. Glycosuria at first resulted from
140 gm. carbohydrate, but by June 16, 171 gm. carbohydrate were taken without
glycosuria. One egg was then added to the diet; and after June 22, 200 to 225
gm. carbohydrate could be taken daily without glycosuria. As a precaution,
however, the allowance was diminished to 150 gm. The diet prescribed at dis-
charge represented approximately 70 to 80 gm. protein (largely vegetable), 150
gm. carbohydrate, and 1200 to 1500 calories (1.5 to 1.75 gm. protein and 26 to 33
calories per kg., without fast-days). As the patient was about 9 kg. below nor-
mal weight, this allowance was considered prudent; and she was permitted to
estimate her diet instead of weighing it, on condition that she be guided by her
body weight and not allow herself to gain much flesh. She was stiU sufiiciently
well nourished to look and feel entirely healthy. The degree of undernutrition
in hospital, and the extent to which fat was excluded and carbohydrate empha-
sized in the diet, can be shown by the following table.

Total.

Average per day.

Calories in diet for 61 days

61,287
2,788.7 gm.
2,073.1 "
7,121.0 "

1005

Protein " " "61 "

45.7 gm.
34 0 "

Fat " " " 61 "

Carbohydrate " " "61 "

117 0 "

Nitrogen in diet for 61 days (Protein -f- 6.25)

446.0 gm.
278.6 "
266.5 "

7 ^ CTTYl

" " " " 49 " ( " ■^6.25)

5.68 "
5 44 "

" in urine "49 "

" " " per kg. per day (average 44 kg.)

0.125"

It should be borne in mind that the diet was strictly vegetarian, chiefly green
vegetables, except for a single egg daily after June 16. A considerable propor-
tion of the protein was therefore non-absorbable, so that the close correspondence

CASE RECORDS 197

between food and urine nitrogen must be attributed not to unusually good utili-
zation of food, but rather to loss of body nitrogen. Protein restriction to this
degree was doubtless unnecessary, but the rigid undernutrition was a commendable
feature.

Subsequent History. — The patient led a thoroughly normal and comfortable life,
but managed her diet so as to permit a gradual gain in weight. Occasional traces
of glycosuria returned, and these and the gain in weight were not checked by mod-
erate exercise which was advised. Presumably eating was increased in propor-
tion to the exercise. During the 2 years outside the hospital the patient had
been married and divorced, and though the glycosuria was attributed partly to
worry, it probably was essentially of dietetic origin. The predominant difficulty
consisted in traveling and hotel life, where vegetables were often cooked with
starch and even sugar. Though feeling perfectly well, she reentered the hospital
for observation on request.

Second Admission. — ^Jime 6, 1916. Weight 49.2 kg. The urine showed a
trace of sugar which cleared up readily without fasting. The carbohydrate
tolerance was not accurately tested, but was evidently somewhat lower than
before.

The patient was dismissed June 20, weighing 48.1 kg., on a diet of 60 gm.
protein, SO gm. carbohydrate, and ISOO calories, with fortnightly fast-days.
The first blood sugar analyses were made during this period, and showed a ten-
dency to slight hyperglycemia.

Subsequent History. — The patient remained free from glycosuria while keeping
house for herself. She then traveled again and gained moderately in weight.
The traces of glycosuria which finally returned were again due to unintentional
irregularities in diet in hotel life.

Third Admission. — Apr. 16, 1917. Weight 46.4 kg. Heavy glycosuria, slight
ferric chloride reaction, ammonia nitrogen 1 .96 gm. , blood sugar 0.317 per cent, CO2
capacity 46 vol. per cent. Glycosuria continued on the diet formerly prescribed,
but ceased with a single fast-day, Apr. 22. A carbohydrate test thereafter
showed a tolerance of only 50 gm. The acidosis meanwhile cleared up. A
carbohydrate-free diet was then instituted, with 65 gm. protein and 1200 cal-
ories. On this there was an excretion of 0.8 to 1 gm. ammonia nitrogen daily.
The last blood examination on May 23 still showed hyperglycemia of 0.176 per
cent. The patient was discharged May 30, 1917, weighing 45.8 kg., on the diet
above mentioned (1.4 gm. protein and 26 calories per kg.). She was to return to
the hospital within a few months for observation to determine whether these meas-
ures were adequate.

Remarks. — One feature of interest is the possible origin of the diabetes from
an infection or operation. Possibly this was no more than an exciting cause.
At any rate, the diabetes was permanent. The case was of the most acute type
and the progress very rapid, so that physicians had given a prognosis of only a
few months of life. The actual result has been an approximately normal exist-

198 CHAPTER III

ence for SJ years to date. The principal trouble has been that the life was too
nearly normal. Though the patient was strictly faithfiil in her intentions, she
led a rather strenuous life and exceeded her diet quantitatively in such manner
that the weight was not held down to the desired degree of undernutrition. The
greatest difficulty has been the prolonged life in hotels, where undue quantities of
carbohydrate were eaten unintentionally. Such causes of injury are very serious
in a case inherently so severe and so susceptible to harmful influences. In addi-
tion, there is the fact that the tendency to hyperglycemia was not detected and
checked in its incipiency. These various causes suffice to account for the clearly
perceptible downward progress. Comparison between the great rapidity of such
progress before beginning treatment, and its slowness during more than 3 years
of still imperfect treatment, casts doubt upon the existence of any "spontaneous"
cause. The patient is stiU comfortable and looks the picture of health. The
more rigorous dietary restrictions now necessary will reduce her considerably in
weight and strength, and it remains to be seen whether they will succeed in
arresting the downward tendency.

CASE NO. 4.

Male, age 12 yrs. American; no occupation. Admitted June 22, 1914.

Family History. — Mother is well. Two of her grandparents died supposedly of
Bright's disease, at age above 60. Her father died supposedly of typhoid at
62. Her mother died of cancer of the stomach at about the same age. Her
only brother and sister are living and well. Father's grandparents died in old
age. Father's mother died of heart trouble at above 70 years. His father died
after 60 with some form of nervous and mental trouble along with glaucoma.
An uncle of the father died at the age of 6 years of diabetes. Two brothers of
the father died, one in Europe at the age of 21, supposedly from overstudy, the
other of some nervous or mental trouble in a sanitarium. The father is the only
survivor of his family and is neurotic. Patient's parents married when the
mother was 19; she had two children 13 months apart and had typhoid when
the first baby was 1 month old; no miscarriages. The first child developed
diabetes at the age of 2| years and died from it at 4 years.

Past History. — Patient had normal birth. Mother's milk disagreed and baby
was raised on artfficial food. At the age of 2 months, history of swelling of both
sides of neck; incisions on the two sides said to have liberated enough pus to fill a
drinking glass; no return of anything of the sort. The baby was healthy and fat,
but not abnormally obese. Several attacks of bronchitis in infancy, "rheuma-
tism" in the legs for 4 days when 4 years old, measles at 5, chicken-pox at 6,
several attacks of tonsillitis thereafter, but no complaint of tonsils in recent years.
In general a bright, healthy, active boy. He attended school for 2 years, there-
after was taught by governess at home. Candy was forbidden from fear of
diabetes, otherwise an ordinary diet was taken with ordinary quantities of
starch.

CASE RECOEDS 199

Present Illness. — Polyuria and polyphagia began at the age of 5, and diabetes
■was immediately diagnosed by family physician. Diet was restricted by with-
drawal of sugars and most starches, substituting gluten bread, but through
more than a year of such treatment patient never became sugar-free. A diabetic
specialist was then consulted and glycosuria was kept absent for several weeks.
Acidosis was found about this time, and a small amount of carbohydrate was then
allowed. He remained under careful treatment up to the age of 9, but felt so
badly and lost so much weight on carbohydrate-free diet that a change seemed
necessary. He was then given liquid diet, taking two or three quarts of milk a
day, but glycosuria became so heavy that strict diet was resumed within a few
days. One such period has been tried since; otherwise a moderately restricted
diet in weighed quantities has been taken. The usual oat cures, preceded and fol-
lowed by vegetable days with eggs have been used repeatedly, but no fast-days.
The patient's highest weight was 70 pounds at the age of 10. Up to the age of
1 1 the urine had been free from albumin so far as observed. At that time both
glycosuria and acidosis became worse, and urine showed considerable albumin and
casts. Nephritis has been present ever since, with more or less edema most of
the time. Vision began to be blurred several years ago and was not aided by
glasses. About a year ago there began to be a mist before his eyes, which has
increased to nearly total bhndness. The hair has been falling out since about
the same time. Teeth have not decayed, but have failed to develop; two ca^-
nines appeared about a year ago and barely protruded beyond the gums. Con-
stipation is complained of, also attacks of vomiting. Coma has been, seriously
threatened on two occasions and has been averted by the free use of carbohy^
drate and alkali. A number of different climates and mineral springs have been
tried without result. Neuritic pains in the legs are also complained of, and on
two occasions recently sUght superficial injuries have produced long-standing
ulcers, one of which is barely healed. The gums are said to bleed whenever the
teeth are washed. The patient has been bed-fast for a month or more on ac-
count of weakness, but recently has been sitting up and dressed for a few hours
daily.

Physical Examination. — Height 140 cm., weight 23.8 kg. Extreme emacia-
tion and weakness. Hair cream-colored, long, silky, thin. Eyelids droop with
look of exhaustion; intraocular tension diminished. Pupils react to both light
and distance, but tests of vision show that only marked changes in illumination
are perceived and only large objects dimly distinguished. Vision better at
periphery than at center of fields. Ears and nose normal. Mouth shows above
mentioned condition of teeth, well kept, but tongue moderately coated. Palate
and fauces narrow; only slight tonsillar enlargement. Palpable glands in neck,
very small. A few sudamina especially on sides of neck. Otherwise skin is dry
and slightly scaly. Knee jerks barely obtainable, other reflexes normal. General
examination otherwise negative.

Treatment. — On June 23 and 24 diet was permitted according to description of

200 CHAPTER in

what had previously been taken. Fasting was begun with some misgivings on
account of the extreme weakness, and whisky was administered in the small
quantities which the patient could take without complaint of discomfort. By
June 27 the strength seemed greater rather than less. Nevertheless as a pre-
caution, since fasting had not heretofore been imposed upon any patient as danger-
ously weakened as this, it seemed conservative on this day to allow 155 gm.
olive oil with a trifle of vegetables as a rehsh. Alcohol was given the next day,
and on the following days olive oil was again added. Green vegetables were then
added, representing carbohydrate as follows: July 1, 6 gm.; July 2, 12 gm.; July
3, 15 gm. A change was then made to protein-fat diet, increasing up to 61.6
gm. protein and 1530 calories on July 13. Pancreas was fed at this time as noted
below. This diet was tolerated as far as glycosuria was concerned. The bare
traces of glycosuria Umited to certain portions of the day, which appeared so en-
tirely unaccountable at that time, were explained subsequently as due to sur-
reptitious eating, in this instance probably of a sweetened tooth-paste. On ac-
count of these traces of glycosuria and the persistent acidosis, an absolute fast
was imposed notwithstanding weakness, and continued for 5 days, being followed
by the alcohol day of July 19, and then by a limited protein-fat diet, always below
900 calories. By the end of this period, Aug. 7, the strength was far better than
at any previous time. The patient was up and dressed most of every day,
walked about the hospital, and on Aug. 7 was strong enough for an automobile
ride. Beginning Aug. 9, a period of very low diet consisting largely of alcohol
and green vegetables was instituted, particularly for the purpose of clearing up
acidosis, until on Aug. 17 one egg was added to the whisky and vegetables. The
diet was increased by one egg daily, tiU on Aug. 20 four eggs were given. After
a fast-day with alcohol on Aug. 24 and a vegetable day on Aug. 25, protein-fat
diet was begim and rapidly increased to 1600 to 1700 calories, with as much as
SO to 60 gm. protein. Glycosuria was stopped by the fast-days (with alcohol) of
Sept. 5 and 6, but returned promptly with resumption of the high diet. It also
persisted during the 2 alcohol days, Sept. 16 and 17, and the low protein-fat diet of
SOO calories or less of the latter part of Sept. and the &st of Oct., but cleared up
■when a diet was subsequently given composed of little more than alcohol and
olive oil. The patient became very weak in consequence of this undernutrition.
On Oct. 19 he woke up weak, but with normal consciousness. While he was
eating breakfast consciousness gradually failed, and within less than an hour he
was entirely unconscious. Pulse and respiration showed no special change.
Tube feeding was instituted, a total of nine eggs and 30 cc. whisky being given in
divided doses. Saline solution was given intravenously at intervals, and three
doses of 10 gm. levulose each in 200 cc. solution were given subcutaneously. Bene-
fit was only temporary, and death occurred after very gradual decline on Oct.
20, with continued imconsciousness but no other signs of diabetic coma and with
urine negative for both sugar and acetone bodies.
Acidosis. — The patient entered with a daily excretion of approximately 18 gm.

CASE RECORDS

201

total acetone bodies (as |8-oxybutyric) and 2.5 gm. ammonia; these were brought
gradually to an almost normal level. A slightly high ammonia and occasional
traces of ferric chloride reaction persisted. Radical treatment of the acidosis
was difficult because of the extreme weakness of the patient.

The results of attempting to maintain strength by the use of fat are shown in
Table V.

Oil days instead of fast-days were tried at the outset as shown, because of their
use by former workers and because of the patient's weakness. The first and

TABLE V.

Diet.

1

fe.

6

S

3

o
gm.

4J

u

i

Urine.

Date.

1

i

1

1

1

1

i

I

CC.

i

1
*3

3

1

U (A

Hi >,

III

1914

em.

gm.

gm.

gm.

gm.

gm.

gm.

gm.

June 23

70.5

101

4.15

—

1623

23.8

—

—

3174

42.51

11.59

1.65

8.00

" 24

91.5

177

103.3

—

2319

23 .'2

—

— .

2772

32.60

10.64

3.44

15.59

" 25

—

—

—

16.5

116

23.2

3

—

2953

12.96

6.67

2.75

9.22

" 26

—

—

—

19.5

137

22.3

—

—

2361

6.85

5.15

2.60

7.67

" 27

6.9

248

11.9

1.2

1578

22.4

—

—

2028

16.30

5.17

2.33

17.81

"" 28

2.3

2.3

1.9

25.5

189

21.2

20

. —

2074

8.90

5.68

2.70

8. 95

" 29

—

50.0

—

26.0

632

22.0

—

5

2238

1.17

3.18

1.80

2.99

" 30

—

80.0

—

22.0

874

21.6

—

20

2483

0

3.50

1.79

4.77

July 1

2.1

102.6

5.8

20.0

1125

21.6

—

20

2153

+

3.61

2.37?

3.25

" 2

5.3

110.0

12.7

10.0

1201

21.0

—

5

1589

0.66

3.18

2.07

2.10

" 3

4.5

12.5

15.3

22.5

353

21.4

—

—

1324

3.92

2.70

1.32

4.35

" 4

7.6

38.0

—

21.2

532

21.6

—

—

1501

-1-

3.33

1.08

7.03

" 5

15.4

12.1

—

11.2

625

21.2

—

—

1340

0.80

3.08

2.20

8.19

" 6

15.4

52.1

—

17.5

669

21.6

—

—

1574

0.97

2.44

1.65

4.35

" 7

22.6

58.1

—

17.5

731

21.4

—

—

2855

0.36-1-

5.47

1.62

7.45

" 8

22.6

58.1

■ —

17.5

731

21.8

—

20

1736

-1-

2.83

1.15

7.23

u 9

22.6

58.1

—

17.5

731

22.6

—

—

2453

-t-

3.48

1.52

5.80

" 10

22.6

58.1

—

17.5

731

22.8

—

—

2749

+

3.33

1.48

5.87

" 11

30.8

82.2

—

17.5

1012

23.2

—

—

2769

+

3.75

1.47

11.66

" 12

30.8

82.2

—

17.5

1012

23.4

—

20

2467

+

4.29

1.26

6.26

" 13

61.6

124.4

—

17.5

1531

23.2

—

18

2768

+

7.94

1.55

6.28

« 14

Fast-day.

—

23.5

—

—

1031

-t-

3.25

0.59

3.37

" IS

u

1.5

23.0

—

—

1082

0.46

2.49

0.62

4.92

" 16

iC

22.6

—

—

1225

0.22

2.47

0.70

3.24

" 17

(t

22.0

—

—

1263

0

"2.70

0.69

0.79

" 18

tt

21.6

—

—

1130

0

1.92

0.28

1.46

" 19

u

12.0

21.6

—

—

1322

0

1.98

0.27

1.09

202 CHAPTER m

largest of such fat rations, on June 27, caused the acetone body excretion to rise
suddenly from 7.67 to 17.81 gm. The next day, without fat, there was an equally
sudden fall to 8.9S gm. The influence of smaller quantities of fat on subsequent
days was less clearly distinguishable, but the general effect was an elevation
of the ammonia and acetone body output, as shown especially by the fall with
fasting after July 13, It is thus evident that even moderate quantities of in-
gested fat keep up acidosis, presumably by maintaining a higher fat metabolism
than on fasting. Also, strength is not improved by such use of fat. On the
contrary, acidosis tends to produce more marked asthenia than undernutrition.
The occasional alkali dosage is shown in Table V. Perhaps the reason for the
absence of increase of ammonia excretion with the high fat intake of June 27, is
that the ammonia formation was already at the maximum possible in this patient
at this level of total nitrogen excretion. Possibly the lack of neutralizing sub-
stance was responsible for the marked clinical symptoms of acidosis (hyperpnea,
prostration, small rapid pulse) which came on promptly toward the close of
that day. It therefore seemed advisable to give 20 gm. sodium bicarbonate
on the next day. Calcium carbonate might theoretically neutralize acid in the
stomach and perhaps to some extent in the intestine. It is not known whether
it served any practical usefulness in this or other cases where it has been tried.
No other alkali was given except toward the close of the history; then on 6 days
(Oct. 8 to 13) without s3rmptoms suggesting acidosis and merely with a vague
idea of guarding against salt starvation, the following mixture was given daily:
sodium bicarbonate, calciimi carbonate, magnesium oxide, each 2 gm., potassium
bicarbonate, 1 gm. The giving or withholding of such mixtures has had no per-
ceptible influence upon this or other patients. Vegetables presumably furnish
sufficient quantity and variety of bases.

Tolerance. — This was exceedingly low, but an exact estimate of it is prevented
by slips in the diet. At the outset, the barely perceptible traces of glycosuria
in the early days of July seemed perplexing. Later, unaccountable glycosuria
was encountered on certain days without clear relation to the known food in-
take. It had seemed that a blind boy isolated in a hospital room and so weak
that he could scarcely leave his bed would not be able to obtain food surrepti-
tiously when only trustworthy persons were admitted. It turned out that his
supposed helplessness was the very thing that gave him opportunities which
other persons lacked. Even on a diet which satisfied his appetite according to
his own statement, as at the end of Aug. and the first of Sept., the attempt to
evade the strict watch kept over him appealed to him as a sort of game or battle
of wits, so that he even took things for which he had no real desire. Among these
unusual things eaten were tooth-paste and bird-seed, the latter being obtained
from the cage of a canary which he had asked for. Also his mother and his
governess on visiting him sometimes brought lunch, which was kept in a closet
supposedly without his knowledge; nevertheless, in the short intervals when he
was unwatched, he managed to find it and remove such articles as might not be

CASE RECORDS 203

missed. These facts were obtained by confession after long and plausible denials.
The experience illustrates what great care is necessary if records of diabetic
patients are to be vouched for as correct.

Weight and Nutrition. — Weight at admission 23.8 kg., at discharge 18.1 kg.
One feature is the successful carrying through of two periods of inanition in a
dangerously weak, small boy. The olive oil, as mentioned, probably did more
harm than good. The whisky may have been of some slight aid, but there was no
plain clinical evidence. The 6 days of almost complete fasting beginning July 14
were borne without signs of collapse, even though the weakness was such as to
cause concern before any fasting was imposed. The diet of some 700 to 800 cal-
ories, protein, fat, and alcohol, in the latter part of July and the first part of
Aug., was theoretically sufficient for maintenance, but was barely tolerated.
Even though some of the glycosuria may have been due to slight errors in diet,
the recurring traces of ketonuria show that this intake was excessive. The
period of carbohydrate and alcohol beginning Aug. 9 cleared up the ketonuria,
but did not avail to prevent its prompt return when a high carbohydrate-free diet
was next attempted. The diet of 1600 to 1700 calories at this time was very
high for this body weight; there was in fact a slight gain of weight and strength,
but as usual the increasing glycosuria and ketonuria forced a cessation of this
plan, and the end-result, as is invariably the case, was harmful instead of bene-
ficial. The subsequent undernutrition beginning Sept. 16 was improperly planned,
because the persistent glycosuria apparently indicated a remarkable absence of
assimilation, whereas the real trouble was the unusual ingenuity of the patient in
obtaining forbidden food.

Pancreas Feeding.— This patient developed a liking for raw pancreas, so that he
spontaneously asked for it. It was therefore of interest to study the effect of a
diet in which pancreas protein was the sole possible source of sugar; i.e., a diet
composed of nothing but pancreas, olive oil, and alcohol. This was the character
of the diet beginning July 4; on that day SO gm. of fresh pancreas weregiven as
the only protein. The next day this was increased to 100 gm., which continued
to July 7, when it was raised to 150 gm. This continued to July 11, when it was
increased to 200 gm. On July 13 the quantity was increased to 400 gm. The
traces of glycosuria were not cleared up either by pancreas or by fasting until
the patient's trick of eating a small quantity of tooth-paste each morning was
detected, whereupon on July 17 the traces of sugar ceased promptly. It is there-
fore evident that pancreas feeding did not avail to establish an assimilation for
even the trivial quantity of sugar contained in a very few grams of tooth-paste.
On July 20, after fasting, the first diet given consisted of 80 gm. fresh beef pancreas
with whisky and olive oil. On July 21 the pancreas was increased to 120 gm.
On July 22 it was only 96 gm. by mistake, on July 23, 120 gm. On July 24 and
25 the identical diet was given, with substitution of raw beef for pancreas. On
July 26 and 27 the same quantity of beef was given, cooked before eating. On
July 28 and 29, 120 gm. of raw pancreas were again substituted. The occasional
glycosuria up to this time was irregular and probably due to surreptitious eating.

.204 CHAPTER in

This diet was apparently near the verge of tolerance. After a fast-day on July
30 the same diet was given, of 120 gm. pancreas with addition of one egg; this diet
continued to Aug. 8. A regular and persistent glycosuria was the result, evidently
■due to the fact that this diet was slightly in excess of the tolerance. It would
therefore appear that fresh pancreas was not able to increase the patient's protein
tolerance to the extent of one egg, since he was mostly sugar-free on pancreas or
raw or cooked beef without the egg, and excreted small quantities of sugar on raw
pancreas with addition of the egg. There was also no perceptible influence upon
acidosis. Another pancreas feeding experiment was tried, begiiming Sept. 10,
with similar result (see Chapter IV).

Remarks. — This 12 year old patient, admitted after 7 years of downward prog-
ress, delayed but not stopped by the most competent care obtainable, with reti-
nitis and profound emaciation and weakness, may be said to have been in the hope-
less stage of his disease. It is of interest that both albumin and casts cleared up
under treatment; they may therefore be attributed to the diabetes or perhaps
:to the acidosis, since true nephritis does not thus disappear. The weight was
reduced by 5.8 kg. in the 4 months of treatment. The improvement in strength
was evident to all concerned and considerable encouragement was felt at one time.
The essential difficulty lay in the stealing of food; on account of this deception
the treatment was improperly managed in several respects. The undernutrition
period of the closing month was what brought on death, which may be attributed
to inanition.

It seems unprofitable to speculate how long or in what condition this patient
might have hved if he could have been treated by undernutrition from the first
-diagnosis of diabetes. What is certain, however, is that diabetic retinitis has
never yet been known to develop under thorough treatment by this method; and
anyone making use of high diets for the sake of supposed comfort must be pre-
•pared to assume responsibihty for occasional blindness and similar troubles.

CASE NO. 5.

Male, married, age 34 yrs. American; customs inspector. Admitted July
15, 1914.

Family History. — Entirely negative for heritable or metabolic disease.

Past History. — Generally healthy life. Measles, tonsiUitis, and adenoids in
childhood. Neisser infection at 22. No history or indications of syphiUs. Ner-
vous and easily excitable since boyhood. Indigestion and constipation began at
about 22 and have grown worse up to the present, probably aggravated by irregu-
lar eating since entering customs service at 23. There is a feeUng of hunger with
nausea between meals, temporarily relieved by eating; no pain, no vomiting, little
• eructation. No alcohol up to 25, then began to drink beer and other liquors,
occasionally to sUght excess; during the past 4 months has lost all appetite for
liquor. Smokes two or three cigars a day.

Present Illness.— In July, 1913, while at work, patient experienced a sudden
-feeling of dizziness, then compression about chest, followed by vomiting, colic,

CASE RECORDS 205'

and diarrhea. After a doctor had given him calomel and salts at home, on diag-
nosis of "autointoxication," he had hot fever during that night, but felt well the
next day and returned to work. Urine was not examined. From that time on
he felt constantly thirsty and steadily lost weight and strength. About Sept. 1
the same doctor was consulted again and found 4 per cent glycosuria. Patient
followed the routine restricted diet prescribed, but was sugar-free only twice for
about a week; this sugar-freedom was obtained by rigid exclusion of carbohydrate.
Acetone appeared, so a small quantity of carbohydrate was allowed, with result-
ing glycosuria. Occasional vegetable days have been employed. Lately a quart
of mUk daily has been added, and diet has been unrestricted on 1 day each week..
On vacation in the country, July of this year, he took ordinary mixed diet for 1
week, and experienced an acute attack similar to the initial seizure 1 year pre-
viously. At present he follows the diet with restricted carbohydrate; feels ner-
vous and weary, no polyphagia, slight polydipsia and polyuria; no dryness of skin,
but on the contrary troublesome sweats. Normal weight has been 175 to 18&
pounds; recently it has fallen to 144 pounds.

Physical Examination. — Height 1 73.8 cm. Weight 60.4 kg. Body well formed,
but lean. Neurasthenic manner, expression indicating weakness and weariness.
Skin very moist, noticeable pallor. Slight enlargement of tonsils. Knee jerks-
entirely absent. Other reflexes normal. Examination otherwise negative.

Treatment. — On the day of admission and the 2 following days, patient was
allowed to choose a diet resembling his habitual one. Then 2 plain fast-days were
given, followed by 3 alcohol days. The result, as shown in the graphic chart,
was a clearing up of glycosuria but persistence of the ferric chloride reaction.
Green vegetables were then added (July 23 to 27) and the latter reaction thus
cleared up. After a single fast-day with alcohol on July 28, the patient proved
able to tolerate a diet as high as 1100 calories with about 50 gm. protein and 70
to 75 gm. carbohydrate. This was undernutrition, representing, for a body weight
of about 60 kg., about 0.9 gm. protein and less than 20 calories per kg. Alcohol'
was discontinued on Aug. 5, as it was unnecessary and the formation of a habit
was undesirable. Beginning Aug. 11, an experimental period was begun to show
the effect of increasing calories, particularly in the form of fat (see below) . There-
after, it was intended to place the patient upon a proper hving ration preparatory
to dismissal; but on Nov. 9 he suddenly requested discharge to accept a particu-
larly favorable business opportunity. He was therefore allowed to go with
approximate instructions regarding diet, following the plan of not weighing his-
food but judging portions by the eye, and guiding himself by his urinary tests and
particularly by his weight. The diet ordered consisted of protein, fat, and about
100 gm. carbohydrate in green vegetables. The entire treatment was not one of
undernutrition, because he left weighing approximately 1 kg. more than on adibis-
sion to hospital. The relative mildness of the diabetes had not called for the-
most rigorous measures, and the patient was already far under normal weight..
He was instructed never to allow himself to gain weight above 160 pounds.

206

CHAPTER lU

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CASE RECORDS

207

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TABLE VII.

Diet.

Urine.

J

OJ

Date.

,

« .

tn U)

1

'Sd

^

S

I.S

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1914

««.

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gm.

cc.

gm.

em.

Sept. 29

26.4

7.3

82.0

511

8.7

58.8

1375

+

+++

8.06

-4.13

+82.0

" 30

26.3

7.2

82.2

511

8.5

60.0

1975

0

+++

10.51

-6.69

+82.2

Oct. 1

26.2

5.9

75.6

471

7.7

60.8

3035

0

+++

6.80

-2.89

+75.6

" 2

25.7

7.3

80.9

513

8.4

60.6

2900

+

++

5.92

-2.10

+80.9

" 3

26.1

7.4

80.4

504

8.3

60.6

2995

0

+++

8.69

-8.98

+80.4

" 4

24.4

6.6

82.5

499

8.3

60.0

2715

0

+

7.06

-3.43

+82. S

" 5

32.5

13.0

80.0

582

9.6

60.2

3380

0

+

9.06

-4.22

+80.0

" 6

40.1

16.8

73.2

620

10.3

60.0

3195

0

0

8.56

-2.69

+73.2

« 7

44.9

57.8

80.1

983

16.3

60.0

2315

+

0

—

+80.1

" 8

45.5

51.6

84.3

1010

16.5

61.0

2590

0

0

8.38

-1.61

+84.3

" 9

46.1

51.7

82.3

1006

14.7

61.4

3205

0

0

8.46

-1.58

+82.3

" 10

45.5

51.6

84.3

1010

16.4

61.6

2615

0

+

7.95

-1.17

+84.3

" 11

51.5

56.3

82.6

1072

17.3

62 jO

2795

0

0

—

+82.6

" 12

S8.7

61.8

77.0

1129

18.1

62.4

2960

0

0

8.88

-0.14

+77.0

" 13

65.2

96.0

82.0

1495

23.6

62.2

2822

0

+

8.81

+0.98

+82.0

" 14

69.1

128.5

82.1

1814

29.1

62.4

3150

0

0

9.45

+0.83

+82.1

" 15

75.2

163.2

82.1

2161

34.4

62.8

3145

0

0

9.12

+2.05

+82.1

" 16

75. 5

187.3

82.4

2392

38.1

62.8

2895

0

0

7.30

+3.84

+82.4

" 17

81

189

105

2518

39.9

63.0

4280

0

0

9.93

+2.11

+ 105.0

" 18

92

196

104

2621

41.6

63.0

3380

0

0

8.92

+4.76

+ 104.0

" 19

104

195

99

2643

41.9

63.0

3270

0

0

10.20

+5.27

+99.0

" 20

103

194

103

2647

41.7

63.4

3960

0

0

11.56

+3.78

+ 103.0

" 21

104

195

103

2661

42.0

63.4

3160

0

0

10.49

+4.99

+ 103.0

" 22

110

203

124

2851

45.0

63.4

4070

0

+

—

+5.38
(calc.)

+ 124.0

" 23

114

197

121

2646

41.7

63.4

3680

0

0

11.48

+s:49

+ 121.0

" 24

114

220

118

2999

47.0

63.8

4254

0

0

15.31

+ 1.64

+ 118.0

" 25

114

228

120

3073

48.4

63.4

4085

0

0

15.36

+ 1.61

+ 120.0

" 26

113

219

119

2829

44.7

63.2

4487

0

0

14.36

+2.47

+ 119.0

" 27

115

221

123

3128

50.0

62.8

3590

0

+

_

+ 123.0

" 28

112

227

118

3053

48.3

63.2

3810

0

0

_

+ 118.0

" 29

114

228

120

3074

48.8

63.0

3554

0

+

_

+ 120.0

" 30

81

222

39

2556

—

—

1605

0

0

_

+39.0

" 31

78

368

51

3950

—

—

930

0

+++

_

+51.0

Nov. 1

108

193

92

2610

39.4

62.2

3770

0

0

+92.0

" 2

148

292

92

3676

59.8

61.4

3205

0

+

_

+92.0

" 3

165

483

104

5595

90.8

61.6

2865

+

++

_

+104. 0

" , 4

165

482

99

5563

89.4

62.2

2600

+

+

,

+99.0

" S

112

351

93

4099

65.9

62.2

3090

0

+

_

+93.0

" 6

Alcohol 2C

'gm.

140

61.6

2690

0

0

" 7

155

221

119

3177

53.6

59.2

2240

0

0

_

+ 119.0

" 8

114

220

120

3002

48.8

61.4

3880

0

0

_

+120.0

" 9

114

220

120

3002

49.0

61.2

1710

0

0

-

-

+ 120.0

208

CASE RECORDS 209

Overfeeding Experiments. — The patient was peculiarly adapted to experiments
with excessive diets, for though he had never suffered from true diabetic poly-
phagia, he was habitually a very heavy eater. Also his constipation was invinci-
ble, notwithstanding the most enormous fat diets. He took these diets with
relish and without increase of his slight dyspeptic complaints. As indicated in the
laboratory chart, the stools were small, hard, and infrequent, and carmine for de-
marcation was always retained for several days. With the return of diabetic
symptoms in each instance the patient felt so much worse that he was glad to re-
sume a rational diet even at the price of slight continual hunger. The experi-
ments were of practical usefulness in convincing him of the inadvisability of try-
ing to satisfy his appetite, and with this object lesson he has remained faithful to
treatment from that time to the present.

Nitrogen Balance. — The most surprising feature is the remarkable nitrogen
retention, comparable to that described in normal persons by Liithje and in dia-
betics by Falta and coworkers. It is to be recalled that the patient was moderately
emaciated from diabetes and had then been subjected to fasting and low diet,
which had reduced his nitrogen excretion to a low level. Also the diet ia this ex-
periment was liberal in protein, and starting at 64.5 calories per kg. increased to
109 calories per kg. — an extreme surplus for a man at rest in a hospital ward.
With the rapid gain in weight it is not surprising that considerable nitrogen was
stored, but it is remarkable that the low output of 6 to 8 gm. daily was main-
tained up to the sudden increase on Sept. 13, the day before the onset of glyco-
suria, and simultaneously with the appearance of the first decided ferric chloride
reaction. The retention then continued, but to a diminishing extent, notwith-
standing the steady increase in total calories. The diminution of storage may
probably be attributed to the active diabetic symptoms. Notwithstanding the
large quantity of nitrogen stored, the fasting and low diet following Sept. 27
quickly brought a return to the same low nitrogen output as before. Analyses
are not complete for the second period of overfeeding, but the data available
fuUy confirm the results in the first period.

Influence of Body Weight. — The weight was built up in two feeding periods on
different diets. Diabetic symptoms were present at the higher weight in each
instance. The attainment of a higher weight in the second as compared with
the first period of overfeeding may have been aided by the mildness of the symp-
toms on the second diet. This difference makes it clear that weight was not
the sole factor in bringing back symptoms, but the kind and quantity of the
different elements of the diet is necessarily an important factor.

Influence of the Diet. — Both glycosuria and acidosis were brought on by in-
crease of the diet, particularly in fat. The influence of the three elements may
be considered as follows.

1. Carbohydrate. — The glycosuria cannot be attributed merely to carbohy-
drate, because the increase of carbohydrate in the first overfeeding period was
not great, and the quantity on certain days, such as Sept. 23, 25, and 26 with

210 CHAPTER in

heavy glycosuria was actually less than on earlier days without glycosuria. Also
in the second overfeeding period the carbohydrate was regularly higher than in
the first one, yet glycosuria was trivial in comparison with the first period. On
the other hand, carbohydrate was not effectual in preventing acidosis, so that
it would have been impossible, even in this relatively mild case, to control acidosis
by feeding carbohydrate along with a high fat diet. A fallacy of the carbohydrate
balance plan is also illustrated; for in the period Sept. 11 to 19 this balance was
as high as before, yet the beginning ferric chloride reactions and the higher average
acetone excretion, though so slight as to be often ignored, were actually significant
of the damage already done by fat and soon to be more manifest.

2. Protein. — Protein was increased at the time of glycosuria and acidosis in
the overfeeding period. Such increase did not prevent acidosis. The gener-
ally higher protein may be regarded as one cause of the heavy glycosuria in the
first overfeeding period, as compared with the slight glycosuria in the second.
On the other hand, protein can scarcely be credited as the sole cause of the gly-
cosuria, since the latter was out of proportion to the increase of protein in the
first overfeeding period, and also on certain days of the second period {e.g. Nov.
3 and 4), with sUght glycosuria, both protein and carbohydrate were higher than
on certain days in the first period {e.g. Sept. 20, 23, 25, and 26) with very heavy
glycosuria.

3. Fat. — The principal increase in the diet was in the form of fat, and to this
may be attributed most of the gain in weight and return of all diabetic symp-
toms. The fat diet was much higher in the first than in the second overfeeding
period, and the excessive caloric intake in this form may be considered the most
important factor in the production of both glycosuria and acidosis. Periods of
fasting and lower diet quickly cleared up both the laboratory and the clinical
symptoms.

4. Calorimetry. — ^This patient was studied by Dr. Eugene DuBois in the
respiration calorimeter of the Russell Sage Institute of Pathology on Oct. 30 and 31
and Nov. S, with a view to observing any possible anomalies in the disposal of
the huge rations, particularly of fat. No departures from the normal were demon-
strated either in the basal metabolism or in that following a heavy fat meal.'

Subseqiient History. — ^The patient remained at work in excellent condition, until
he reported at the hospital on Dec. 28 weighing 160 pounds, glycosuria having
come on with the increase in weight without change in the prescribed diet. Fast-
ing and reduced diet at home brought him down to 157 pounds, but a trace of
sugar returned on Jan. 10. He was therefore instructed to keep his weight there-
after below 155 pounds. He then remained continuously sugar-free until he re-
ported at the hospital on Mar. 21 with the following history. On account of
his slight indigestion he had consulted a well known stomach specialist of New
York, who told him that he must omit most of his vegetables and take two white

1 Cf. Allen, F. M., and Du Bois, E. F., Arch. Int. Med., 1916, xvii, 1010-1059.

CASE RECORDS 211

rolls daily. The patient objected that this would bring back his glycosuria,
but the physician responded that he had better have glycosuria and feel better.
The patient therefore took the white rolls for a short time, and promptly showed
heavy glycosuria. He then on his own judgment stopped the rolls, cleared up the
glycosuria by fasting, and reported at the hospital because his tolerance had
been lowered and he now showed traces of sugar on the diet on which he was for-
merly sugar-free. A reduction of his green vegetables was therefore ordered, and
he was instructed not to exceed his existing weight, which was then ISO pounds.
At this weight he was reasonably weU nourished and fully able to work, and his
troubles were all classified as neurasthenic.

On Apr. 2 and again on Apr. 9, the patient reported, showing both sugar and
ferric chloride reactions and weighing 149 pounds. The vegetables were ordered
thrice boiled so as almost entirely to exclude carbohydrate from the diet, and the
quantities of food were now more strictly regulated so as to make a ration of
approximately 2500 calories.

On June 19, the ferric chloride reaction was negative, but there had been traces
of glycosuria from time to time.

On July 13, he returned with a similar report, but had recently caught cold,
and this had brought a return of glycosuria, concerning which he was very nerv-
ous. He was therefore readmitted to the hospital for the week July 13 to 19
for purposes of instruction. Physical examination was as before, except for en-
largement of the hver to 5 cm. below costal margin. He was placed on a diet
of approximately 2100 calories, with 90 gm. protein and 30 gm. carbohydrate
(see graphic chart). He was discharged with instructions to weigh all food,
adhere rigidly to this diet, and take a fast-day once every week.

On Aug. 8, he weighed only 58.8 kg., and complained of weakness, weariness,
and hunger, but had shown no sugar since leaving hospital. Bran muffins were
added to relieve both his feeling of emptiness and his constipation.

On Feb. 28, 1916, the report was similar. He was walking 6 mUes daily for
exercise. On this basis his diet was increased to 108 gm. protein, 30 gm. carbohy-
drate, and 2400 calories. Thereafter he continued at work with favorable re-
ports until June 5, when the carbohydrate was increased to 40 gm. and the cal-
ories to 2500. Traces of glycosuria gradually came on, so that on July 17 the
carbohydrate was again reduced to 30 gm.

The urine subsequently remained free from both sugar and ferric chloride
reactions, and the patient gradually increased his exercise to 8 miles of walkiag
daUy.

On May 23, 1917, the weight was 56 kg., the blood sugar 0.116, and the car-
bon dioxide capacity of the plasma 59.9 per cent.

On June 13, 1917, the weight was still 56 kg. and diet was 20G0 calories, with
50 gm. carbohydrate and 70 gm. protein. The blood sugar was 0.155 per cent,
and the carbon dioxide capacity of the plasma 64 per cent. The urine remained
negative for sugar and ferric chloride reactions.

212 CHAPTER III

Remarks.— This was one of the early cases, and the treatment contained errors
accordingly. The diabetes was of moderate severity, and the attempt was made
to treat it with as little inconvenience to the patient as possible, insisting upon
a normal urine and a moderately reduced body weight, and hoping for a recovery of
assimilation under these conditions. The result shows that such loose methods
are not advisable even in a case of this type, and that tolerance is lost rather than
gained under such a plan. The patient had felt unable to work at the time of his
first admission to hospital. He has been kept in working condition during most
of the time for 3 years. His tolerance has fallen sUghtly, so that now about
80 gm. carbohydrate is tolerated with a diet of 2200 calories. The blood sugar was
never reduced to normal, as might easily have been done, and the slight downward
progress seems to be nothing inherent in the nature of the condition, but rather
due to the inadequacy of the treatment and the continuous shght overtaxing of the
assimilation. On the whole, a prolonged and conscientious attempt was made to
treat this case from the standpoint of immediate comfort and efficiency, and the
record is now believed to show that this treatment is unjustifiable even for a case
apparently as well suited for it as this one.

Recent examinations have shown that the liver, which was normal in out-
line at the first examination, and afterward was obviously enlarged in examinations
by different observers several months apart, is now distinctly subnormal in size.
The superficial veins of the abdomen are becoming prominent. The diagnosis
of cirrhosis seems evident, progressing through the hypertrophic to the atrophic
stage. This has not suppressed the diabetes and dietary care should not be
remitted, but the most rigorous measures appear unnecessary. The frequency of
pancreatitis in connection with cirrhosis of the liver is worthy of investigation.

CASE NO. 6.

Female, married, age 48 yrs. Italian; housewife. Admitted July 23, 1914.

Family History. — Indefinite. Patient is ignorant of any special disease in
family. (Husband, short and obese, is said to have developed mild diabetes
siince this patient's discharge.)

Past History. — Very healthy life. Patient keeps house for her husband and
four children. Six children died young, perhaps because of tenement conditions.
One of those living is mentally defective. Menses regular up to 1 year ago,
absent since. She drinks four glasses of beer, one cup of coffee, and one cup of
tea a day. Other habits are those of an industrious poor Italian woman.

Present Illness. — Patient was admitted on the pneumonia service on July 23,
1914.

Physical Examination. — ^A short, slightly obese woman with sturdy peasant
appearance, and normal on physical examination except for consoHdation and
pther signs of pneumonia of right lower lobe. The urine showed heavy sugar and
ferric chloride reactions, though there had been no former complaints indicating
diabetes.

CASE RECORDS 213

Treatment was conducted first by the pneumonia service of the hospital. The
temperature fell by lysis on the 5th, 6th, and 7th days, and on July 31 the signs
in the right chest had cleared up and the patient was turned over to the diabetic
service.

During the period of pneumonia the diet consisted of oranges and egg-nogs
with whisky and cream, the caloric intake being about 1400 to 1600, as shown
in the graphic chart. Glycosuria and ketonuria remained heavy during this
time as indicated, but there were no symptoms threatening coma.

Diabetic treatment was begun on Aug. 1 with fasting, with addition of whisky
because of the convalescent condition. She thus received about 600 calories of
alcohol daUy until Aug. 7 to 8. She was a very unwilling patient during this
time, having been content to stay in the hospital during the pneumonia, but now
that she felt well, she was determined to go home to her babies. She had never
heard of diabetes and was accordingly unwilling to be treated. Her husband was
'of equally ignorant type, but fortunately he and certain relatives had seen a
few deaths from diabetes and comprehended the necessity of dietetic treatment.
Accordingly she consented to remain until completion of treatment. On Aug.
8, green vegetables were added to the whisky and gradually increased until on
Aug. 14 they represented 80 gm. carbohydrate. The next day one egg was
given, Aug. 17 two eggs, Aug. 18 three eggs, Aug. 19 four eggs, and the next
■day 100 gm. fish were added. A ration was thus gradually buUt up amount-
ing to some 1400 to 1700 calories, with 100 gm. carbohydrate and almost the
same quantity of protein. This seemed to be an adequate but not excessive
diet for her body weight of 54 kg., and it was tolerated without glycosuria
or ketonuria. She received several days' instruction in the diet kitchen in the
preparation of her food. She was not required to weigh it, but was ordered to
take the same kinds and quantities at home as she had been receiving in the
hospital.

Acidosis.— A small point is noteworthy regarding the effect of alcohol. On
fasting with whisky the ferric chloride reaction became absent on Aug. 3, and
the glycosuria the next day. With continuance of 600 calories of alcohol daily,
the ferric chloride reaction reappeared on Aug. 6. 600 calories of alcohol there-
fore did not suffice to keep it absent. It cleared up on Aug. 13 in consequence
of the addition of green vegetables to the whisky, about 50 gm. carbohydrate in
this form sufficing for this result.

Subsequent History. — ^After dismissal on July 31, nothing more was heard from
the patient until Nov. 25, 1914, when she called at the hospital by request, bring-
ing a specimen of normal urine and reporting that she had followed her diet faith-
fully and that daily urine tests had been uniformly negative. Circumstances pre-
vented testing the carbohydrate tolerance at that time.

Nothing more was heard from her until she was finally located by the
visiting nurse and called at the hospital by request on July 5, 1917. The urine
:showed heavy sugar and negative ferric chloride reactions. The patient claimed

214 CHAPTER in

to feel entirely weU but looked pale and run down. She admitted that she had
abandoned diet shortly after her previous report and since then had eaten starches^
sugars, and the regular family diet without restriction. She was advised to
reenter the hospital and resume treatment, but refused on the ground that her
children required her presence at home.

Remarks. — ^The case is chiefly noteworthy from having been first discovered
during an acute infection. Presumably diabetes had been present without notice-
able symptoms before this time. It was evidently aggravated as usual by the
infection. The case is essentially mild and readily controllable by treatment, but
the patient's ignorance and neglect are responsible for continuance of active
symptoms, which may be expected to bring serious trouble within a few years.

CASE NO. 7.

Female, married, age 36 yxs. American; clothing saleswoman. Admitted
July 23, 1914.

Family History. — Father died at 52 of heart trouble. Mother alive and
healthy. All grandparents lived to old age. Five brothers and two sisters of
patient alive and well. No diabetes or other family disease known.

Past History. — ^Healthy life, but obesity from childhood. Only sickness scar-
let fever. At the age of 15 patient weighed 135 pounds; before onset of present
trouble, her weight was 168 pounds. At 18 she began work as a clothing sales-
woman; married at 33 but continued work. No children; one miscarriage. Un-
happy married life ending in separation. Habits said to be regular, alcohol de-
nied. Patient was a light eater all her life and also indulged very little in candy
or sweet dishes. Since onset of diabetes, for thirst and to stimulate strength,
she has taken coffee to excess, at least 20 cups a day, 1 pound of cofiee every 2
days. Nervous since onset of diabetes but not before.

Present Illness. — Symptoms began last Dec. with pruritus vulvae. A physician
made an examination and prescribed a local application without testing urine.
She and her friends noticed rapid loss of weight, and she applied at the Board of
Health for examination for tuberculosis, which was found absent. She then
went to a medical school clinic, where the physician in charge diagnosed diabetes
and merely gave her a list of things to eat and to avoid. During 4 months' at-
tendance at the clinic no benefit was received, and pruritus vulvae and loss of
weight continued. Since Mar. there has been constant pain in calves of legs,
described as like toothache. Within the past few weeks she has had six styes
on the left eye, which healed uneventfully. Much of her hair has fallen out.
There is polydipsia and polyTiria but no pol3T)hagia.

Physical Examination. — ^Nutrition still medium, though superficial tissues
show flabbiness and wasting. Nervous facies and behavior. Posterior cervical
glands slightly enlarged. Vagina and surroimding parts show superficial in-
flammation. Uterus retroflexed retroverted. Examination otherwise negative.
Wassermann reaction negative.

CASE RECORDS 215

Treatment. — For the first 3 days, the patient was allowed an observation diet
Tunning as high as 115 gm. protein, 80 gm. carbohydrate, and 2000 calories. On
this her highest sugar excretion was 63 gm. The ferric chloride reaction, whicL
was slight on admission, became heavy on this diet, indicating that the former
diet had included more carbohydrate. 2 days of absolute fasting were then im-
posed. The glycosuria ceased but the ferric chloride reaction remained heavy.
The next day 100 gm. lettuce and 100 gm. cucumber were allowed. Green vege-
tables were increased daUy without other food untU 33 gm. carbohydrate were
;given in this form on July 30. The ferric chloride diminished to a shght reac-
tion, but glycosuria appeared. A fast-day with 35 gm. alcohol was then given,
and as glycosuria immediately ceased, 27 gm. carbohydrate in the form of green
vegetables were given the next day for the sake of acidosis. Glycosuria ap-
peared, but the carbohydrate was continued for 2 days. Then Aug. 3 was a fast-
•day with 70 gm. alcohol. On Aug. 4, 12 gm. carbohydrate were given as green
vegetables, and on Aug. 5, 17 gm. The ferric chloride reaction had been di-
minishing and was now absent. Although glycosuria remained absent, Aug. 6
and 7 were fast-days with respectively 65 and 87 gm. alcohol. A slight ferric
•chloride reaction returned. On Aug. 8, 90 gm. alcohol and 5.8 gm. carbohydrate
(in green vegetables) were given. On Aug. 9, the alcohol was increased to 120
gm. and the carbohydrate to 16 gm.; Aug. 10, alcohol 105 gm., carbohydrate 17
gm.; Aug. 11, alcohol 90 gm., carbohydrate 22 gm. The alcohol was then dimin-
ished to, 75 gm. and this program was continued to Aug. 16. The ferric chloride
reaction had been well marked under the large doses of alcohol at the beginning
of this period, but gradually diminished with the introduction of carbohydrate
untU it became negative. On Aug. 17 one egg was added, on Aug. 20 a second egg.
A slow increase of diet was continued, until on Aug. 27 it included four eggs, 200
gm. meat, and green vegetables representing 41 gm. carbohydrate. Both glyco-
suria and ketonuria were now continuously absent, the exclusion of fat having
been the principal means by which this end was attained. Fat was then gradu-
ally introduced, finally making a diet of about 100 gm. protein, 60 gm. carbohy-
drate, and 2100 calories. Slight glycosuria resulted and the diet was therefore
•diminished to 80 gm. protein and 1700 calories.

The patient began to keep irregular hours on visits outside the hospital and
was absent one whole night, returning with glycosuria. On Sept. 28 she went
out and failed to return. She reappeared on Dec. 7 showing 3.3 per cent glyco-
suria, which easily cleared up. She visited friends on Christmas and did not
■return for 2 days. Therefore on Dec. 27 she was dismissed for this conduct, and
no further tracing of her case was attempted. ' The impression was received that
the patient was a drug addict or an occasional alcoholic, and that her behavior
was thus explained, but no real proof of this supposition was obtained.

Acidosis. — ^The only noteworthy feature is the fact that doses of alcohol from
75 to 120 gm. failed to clear up the ferric chloride reaction or prevent its reap-
pearance. The efficient means of stopping the persistent acidosis was found in

216 CHAPTER III

continued undernutrition and carbohydrate up to the limit of tolerance, with-
abstinence from fat.

Remarks. — The initial treatment consisted in continuous undernutrition with
as much carbohydrate as possible. After both glycosuria and ketonuria were
thoroughly controlled, the diet was built up by the gradual addition of first pro-
tein and then fat. The weight at entrance was 52.8 kg. The lowest weight re-
sulting from the undernutrition was 47.9 kg. on Aug. 19. Thereafter it gradu-
ally rose, and at the time of her first leaving on Sept. 28 the patient weighed 50
kg., which was a satisfactory state of nutrition for both comfort and strength.
The case illustrates the treatment of diabetes of moderate intensity with the aid of
only the simplest laboratory tests. The outcome was satisfactory except that
the psychic instability of the patient precluded continuing treatment.

CASE NO. 8.

Male, married, age 29 yrs. American; printer. Admitted July 28, 1914.

Family History. — Father and mother are alive and well. Mother had a goiter
removed at age of 40 for cosmetic reasons; there were no symptoms. Grand-
parents all healthy. Patient is the oldest of six children. No diabetes or other
family diseases.

Past History. — Healthy life. Measles, mumps, and chicken-pox in childhood.
Always took cold easily; never had sore throat. Slight pleurisy 4 years ago; irk
bed only 1 day. Regular life; no excesses Never nervous. Married 1 year ago;
wife well, never pregnant.

Present Illness. — In June, 1913, immediately upon return from honeymoon^
patient noticed abnormal thirst and dryness in mouth. Physician immediately
diagnosed diabetes but merely prescribed a diet list, and condition rapidly grew
worse. Patient was then referred to a New York physician who ordered a diet of
nothing but ham and lettuce. He lived strictly on this diet for 6 weeks, eating
as much as 5 or 6 pounds of ham a day. Sugar diminished but did not disappear.
Other treatments were tried with a steady downward progress. He then con-
sulted a New York specialist, who placed him on strict diet with one " green day""
each week, and three or four teaspoonfuls of sodium bicarbonate daily. The-
urine was never sugar-free, and the loss of weight and strength became worse^
On July 25, 1914, patient entered a New York hospital, where a D : N ratio of
3 : 1 was demonstrated on carbohydrate-free diet. Coma threatened on this diet^
but the addition of a slice of bread seemed to make him worse. He was then-
transferred to this hospital in critical condition.

Physical Examination. — An emaciated man appearing very weak. Face thin,
and nervous. Skin dry. Acetone odor. Drowsiness and increased respiration
very evident. Knee jerks absent. Physical examination otherwise negative.

Treatment. — For the first 4 and a fraction days in hospital, the patient was
placed on an observation diet as nearly carbohydrate-free as convenient, thrice
cooking of vegetables having not yet been adopted. This diet, which represented

CASE RECORDS 217

77 to 135 gm. protein, 6 to 12 gm. carbohydrate, and 2800 to 3300 calories, was
all the patient could eat. He showed the usual inability to gain weight or strength
on full feeding, and clinical evidences of acidosis increased. 20 gm. sodium bicar-
bonate and 20 gm. calcium carbonate were given daily. By Aug. 2 there was in-
cipient coma with nausea, continuous dozing which was promptly resumed when-
ever patient was roused, hyperpnea, malaise, and weakness. Fasting was there-
fore begun from necessity. Whisky was given in 10 cc. doses hourly, amounting
to about 100 gm. alcohol on the various fast-days. Calcium carbonate 20 gm.
and sodium bicarbonate 30 gm. were given on Aug. 2. On Aug. 3 the bicarbon-
ate was increased to 40 gm., on Aug. 4 it was diminished to 20 gm., and on Aug. 5
all alkali was stopped. Clinically, meanwhile, the condition seemed to grow worse
during the first 24 hours of fasting; the sleep was noticeably deeper. Improve-
ment on the following day was marked and all the threatening symptoms cleared
up rather suddenly. Sugar-freedom resulted on Aug. S, the 4th day of fasting,
although the D : N ratio had been 3 : 1 on the feeding days. Because of the
marked weakness, whisky was continued in doses just short of producing intoxi-
cation, and green vegetables were gradually added, beginning Aug. 7 with 100 gm.
each of lettuce and cucumbers. On Aug. 10 the quantity of carbohydrate in this,
form amounted to 38. S gm., and by reason of 240 cc. whisky, the total calories for
this day were 1073. TherewasadayofwhiskyaloneonAug.il. The program
of alcohol and green vegetables was continued to clear up acidosis thoroughly,
and 40 to 50 gm. carbohydrate were now assimilated daily without glycosuria.
The ferric chloride reaction was abolished, but the patient was ravenously hungry
and seriously weak. Accordingly, on Aug. 23 the carbohydrate was stopped, and
the diet consisted of 4 eggs, 100 gm. butter, and 135 gm. alcohol. The eggs were
then increased and the alcohol diminished daily, until on Aug. 27 the diet was 60
gm. protein, 37.5 gm. alcohol, and 1660 calories. Aug. 28 was a "green day" of
nothing but alcohol and green vegetables with 55 gm. carbohydrate. This sort of
program continued until Sept. 11. As usual, no benefit to weight or strength re-
sulted from the attempt to feed to the limit. Accordingly, on Sept. 12 a lower
diet was begun, carbohydrate-free, with 80 gm. protein and 1300 calories, the alco-
hol being at the time diminished to 20 gm. daily. For the weight of about 35
kg. this meant less than 30 calories per kg. daily, and this was diminished still
further by the fast-days every 1 or 2 weeks. Exercise would presumably have
been beneficial, but the tradition was followed of keeping a patient with severe
diabetes as quiet as possible. Therefore he was weak and cold and spent most
of his time in a chair close to the radiator, clad in heavy clothing and double
underwear. Nevertheless, the condition at certain times began to appear rather
promising, since the sugar and ferric chloride reactions were frequently both nega-
tive. A difference from the average case soon began to be noted, in that sugar
kept unaccountably reappearing and the tolerance seemed to be perceptibly fall-
ing under conditions when it should have risen or at least remained stationary.
With the progress of time it became more evident that something unusual was

218 CHAPTER ni

breaking the patient down. Dr. Joslin chanced to see the patient on a visit and
suggested the presence of tuberculosis, but physical signs and sputum examina-
tions remained negative. Dec. 6 to Jan. 1, pancreas and duodenal feeding were
attempted without benefit, as described elsewhere (Chapter IV). Thereafter
the attempt at radical treatment of the diabetes was abandoned, and the patient
was allowed at times to eat his fill of a selected diet. Although this diet amounted
sometimes to 60 or 70 calories per kg., there was the usual absence of benefit
to weight or strength, and the attempt to overfeed was doubtless a mistake.
Certain days of lower diet and occasional fast-days were necessarily inserted be-
cause the increasing acidosis sometimes threatened coma. On Jan. 9 he was
transferred to the metabolism ward of the Russell Sage Institute of Pathology at
BeUevue Hospital for calorimetric studies by Dr. Eugene DuBois.' He returned
to this hospital on Jan. 15. The diet of 2000 calories or over during most of
Jan. failed to prevent further loss of both strength and weight . Both the weakness
and the rapidly falling weight were probably associated with the seriously increas-
ing acidosis. The steep elevations in weight shown in the graphic chart at times
in this same period represented marked edema due to sodium bicarbonate in doses
up to 80 gm. daily. Nevertheless on Feb. 1 the point had been reached where a
choice was necessary between fasting and immediate death in coma. A 6 day
fast with whisky was accordingly imposed, which stopped the glycosuria and
cleared up the threatening symptoms, though the ferric chloride reaction was not
made negative. A lower diet was then employed, mostly about 30 calories per
kg., on which glycosuria remained almost continuously absent and greater comfort
was enjoyed by reason of the absence of acidosis symptoms, though the patient
was very weak. On Mar. 16 the patient had the symptoms of catching cold
with fever and pain in the chest. Some dulness and crepitant rMes were now de-
tected. On account of the aggravation of the diabetes, fasting with alcohol was
employed on Mar. 16 and 17, but the glycosuria increased. The D : N quotient
on Mir. 16 was 2.3, on Mar. 18 it was 4.6. As death was imminent, the attempt
at dietary restriction was abandoned and a liberal protein-fat diet with alcohol
was permitted. By Mar. 22 the weakness had become extreme. Though there
was chemical evidence of intense acidosis, the patient never went into typical
coma. Death occurred at noon on Mar. 22, 1915; the patient recognized his
wife shortly before this, though too weak to speak.

Acidosis. — The intense acidosis during the first days in hospital was mentioned
above. On Aug. 1 the excretion of ammonia was 3.5 gm. and that of acetone bodies
(expressed as ;8-oxybutyric acid) was 38.6 gm. A rapid fall was evident even in
the first 24 hours of fasting. On Aug. 8, with 16 gm. carbohydrate in the diet,
the excretion was still 1.1 gm. ammonia and 3.1 gm. /?-oxybutyric acid. It is
noteworthy that the period of 20 days up to Aug. 23, with a diet composed solely
of alcohol and green vegetables in the quantities shown, failed to clear up the
acidosis entirely, as indicated by the excretion of 0.76 gm. ammonia nitrogen and
0.48 gm. /S-oxybutyric acid on Aug. 22. If allowance be made for the effect of the

CASE RECORDS 219

40 to 50 gm. of carbohydrate, which was assimilated without glycosuria, it would
seem that no evident antiketogenic effect, was exerted by approximately 600
calories of alcohol in the diet daily. A specific character of the acidosis perhaps
is recognizable in such cases, by comparison with others in which acidosis is
absent on similar regimen. Neither carbohydrate nor alcohol, but undernutrition
was the essential factor in controlling the acidosis at all periods of the treatment.

With a rather high carbohydrate-free diet beginning Aug. 23 there was a
marked rise in ammonia excretion, showing the harmful effects of the attempt to
build up strength or weight above the tolerance. With the low diet which began
Sept. 11 there was a gradual improvement, so that even without carbohydrate in
the diet the ferric chloride reaction became entirely negative on Oct. 7, and no
more than traces reappeared during the time of radical treatment. Early in
Dec, when the attempt was begun to nourish liberally on account of the assumed
infection, there is another marked rise in the acidosis, going higher as the attempt
was prolonged, until on Jan. 20 the ammonia excretion reached 5.1 gm. In con-
sequence of 2 fast-days it fell sharply, then rose to 4.62 gm. on Jan. 28 in con-
sequence of further excessive feeding. Then on fasting and lower diet it fell
and remained at a much lower level until near the end, analyses in the last few
days of life being lacking because of loss of some urine.

Beginning Jan. 25, the carbon dioxide capacity of the plasma was also deter-
mined. It is seen that although the body weight at that time was rising in con-
sequence of edema from heavy bicarbonate dosage, the blood alkalinity fell
sharply to a dangerously low level. With the fasting and alcohol beginning
Feb. 1 it rose easily within normal limits, then ranged slightly below and slightly
above the lower normal level for most of the remaining time, but dropped sharply
almost to the coma level just before the fatal end.

A statement of the alkali dosage is necessary for proper interpretation of the
ammonia and COj curves. After the stopping of alkali on Aug. 5 as above men-
tioned, no more was given until Aug. 28. From Aug. 28 to Dec. 18 inclusive, the
patient received daily 2 gm. each of sodium bicarbonate, calcium carbonate, and
magnesium oxide, and 1 gm. potassium bicarbonate. These were given in the
attempt to assure against a deficit or improper balance of any or all of these
bases, as well as to neutralize acids. Similar mixtures have been used in a few
other cases. The points in mind have been the reported wasting of bones and ex-
cretion of bone salts in diabetes, and also the vague idea sometimes suggested that
a disturbance of the balance of salts or metals is at the bottom of diabetes. No
effect of such mixtures upon the tolerance or general condition, and no advantage
over the use of sodium bicarbonate alone, have been perceptible in any of the
cases.

On Dec. 19, 6 gm. sodium bicarbonate were given, and 2 gm. on Dec. 20.
The ammonia excretion following the huge diet of Dec. 30 was less than it other-
wise would-have been, because of the giving of 6 gm. sodium bicarbonate on Dec.
30, and 15 gm. sodium bicarbonate and 30 gm. calcium carbonate on Dec. 31.

CASE RECORDS 221

Present Illness. — 1 year ago patient consulted a physician for a severe cough
which had lasted about 2 weeks, and also for a slight injury to his right knee
due to a fall. He was told that he had "lung trouble" and was sent to the
country. Here he began taking a larger diet than that to which he was accus-
tomed, and especially a great deal of cereals and starchy foods. In about 2
weeks he began to notice polyuria and polydipsia. A physician then diagnosed
diabetes. A list of carbohydrate-free foods, also " Metchnikoff 's tablets" were
prescribed. For the past 9 months he has been under treatment at one of the
best New York clinics on practically carbohydrate-free diet. The severer symp-
toms date back 4 or S months, during which time he has lost 25 pounds in weight,
has grown much weaker, and his cough has become worse. Constipation and
abdominal cramps have been jnarked, with nausea and sometimes vomiting.
There is a chronic cough, mostly at night, with expectoration of white mucus
without blood. There was blood in the sputum on one occasion. He now
drinks 20 to 30 glasses of water daily and passes as much as 8 quarts of urine.
Polyphagia present. "••

Physical Examination. — ^Young man with nervous look, moderate emaciation,
and general appearance of weakness. Eyes unduly bright, face flushed, skin in
good condition. Some pyorrhea, and a few decayed teeth. Throat red, tonsils
not visibly enlarged, cervical glands not palpable. A few subcrepitant riles in
both apices posteriorly, and expiratory murmur slightly prolonged; lung sounds
otherwise normal. Organs otherwise negative. Knee jerks absent. Blood
pressure 80 systolic, 60 diastolic.

Treatment. — The patient was placed upon an observation diet of protein, fat,
and green vegetables for 4 days, as shown in the graphic chart. Glycosuria was
as high as 98 gm. on Oct. 11, but the excretion of acetone bodies was not above
1.4 gm. of /3-oxybutyric acid. Fasting with whisky was begun on Oct. 12, and
the urine became sugar-free on Oct. 15. Nevertheless, as the patient was well
able to endure fasting, green vegetables were not begun untU Oct. 18, when 6
gm. carbohydrate were given in this form, increased to 15 gm. on the next day,
30 gm. on the next, and 54 gm. on the next. Sugar was present in traces on the
last 2 days (Oct. 20 and 21), therefore 1 more fast-day with alcohol was given on
Oct. 22. On Oct. 23 the diet consisted of one egg, 30 gm. alcohol, and 600 gm.
thrice cooked vegetables. The next day was similar, with two eggs and substi-
tution of 20 gm. butter for the alcohol. Three eggs were given on Oct. 25, and
four on Oct. 26, and then fat was gradually introduced in the form of butter and
bacon. A little steak was added on Oct. 30. The highest diets of this period,
Oct. 29 to Nov. 1, were only 40 to 60 gm. protein and some 1200 to 1400 calories.
But the traces of sugar and ferric chloride reactions made a fast-day with alcohol
advisable on Nov. 2. A higher diet was then attempted, up to 2700 calories on
Nov. 12, with 17 gm. carbohydrate and 99 gm. protein. The rise in glycosuria
was controlled by 1 fast-day with whisky on Nov. 16 and 2 complete fast-days
on Nov. 30 and Dec. 1. Protein-fat diets were then employed during most of

222 CHAPTER ni

Dec. and Jan., the short high calory periods being atoned for by other days of
fasting or very low diet. The carbohydrate feeding shown in the graphic chart
for the latter part of Jan. represents caramel, which was tolerated with very little
glycosuria. It was evident from experience that the patient's carbohydrate
tolerance was practically nil, and symptoms returned with any attempt at protein-
fat overfeedmg. Therefore, in Feb. he was placed on a diet of about SO gm. pro-
tein and ISOO calories, which, if the body weight be set at SO kg., would be 1 gm.
protein and 30 calories per kg. A fast-day once a week served to reduce this by
i, making it equivalent to ? gm. protein and 26 calories per kg. Exercise had
not been adopted for such cases at that time, and this patient was kept mostly
at rest. He pronounced this diet adequate for his appetite, and was dismissed
on Feb. 17, free from glycosuria and acidosis and, in condition for taking up some
light occupation.

Subsequent History. — After several weeks experience with the diet prescribed
at discharge, the patient had professed his full ability and willingness to live
on it, and was expected to go to some nearby place in the country and report
frequently concerning his progress. No reports were received. It was learned
that he had told another patient in the ward that he was not satisfied to be re-
lieved by diet. He showed an advertisement of a proprietary remedy for diabetes
and announced his purpose to seek a complete cure. Instead of keeping his
promise to the hospital, he went immediately upon departure to a southern
state. He died in Mississippi on Apr. 17, exactly 2 months after discharge.
This information was received from a life insurance official, who was unable to
give any particulars concerning the death.

Acidosis. — The slightness of ketonuria at admission is presumably to the
credit of the treatment given the patient at the clinic in the previous months.
It was easily cleared up by the routine measures. The acetone body excretion
remained low notwithstanding the high diets in Nov., but the ammonia rose
to apfftoximately 1 gm. on two occasions. It fell after the fast-day with whisky
on Nov. 16, but the fall was particularly sharp in the 2 days of plain fasting,
Nov. 30 to Dec. 1. Acidosis was easily controlled during the hospital stay.
There was no doubt of the inherent severity of the case, however, and the prob-
able cause for death 2 months after leaving hospital symptom-free would
undoubtedly be coma.

Blood Sugar. Renal Function. — The few analyses from Oct. 11 to Nov. 2 indi-
cated that the blood sugar was rather easily brought to normal. Traces of gly-
cosuria appeared with a lower blood sugar level than usual for diabetic patients,
and the findings suggested that the kidney was rather easily permeable. This
is the more interesting in view of the fact that small quantities of albumin and
casts were present in the urine at some times. This patient was also one of
those who, from renal deficiency or unknown cause, are subject to marked
edema under treatment. The sharp rise in weight on fasting and low diet, up
to 56.2 kg. on Nov. 1, was an example of marked edema. Other peaks in the

CASE EECORBS 223

weight curve likewise are explainable as edema, sometimes not visible, but in the
marked instances plainly evident in face and extremities, with pitting about the
ankles. The rapid clearing up of edema with sharp fall in weight as shown at
various points on the chart was regularly accomplished by salt-free diet.

Remarks. — This patient was neurotic and secretive. Most of his difficulties
in the hospital were neurasthenic, and the attempts to please him were responsible
for most of the irregularities and excesses of the diet. He was admitted with
a particular view to the suspicion of tuberculosis. The cough gradually cleared
up during the diabetic treatment. In Jan. he had a 10 day attack of bron-
chitis. Examinations for tubercle bacilli on 6 days of this attack as well as on
other occasions during his hospital stay were uniformly negative. He was kept
in the fresh air most of the time and at dismissal was continuously free from
cough or any perceptible signs in the chest. The diagnosis of the pulmonary
condition is therefore uncertain.

The entire lack of ability to take carbohydrate without glycosuria on a diet
of less than 30 calories per kg. is one index of the severity of the case. Theoreti-
cally, some degree of tolerance should have been built up by more radical under-
nutrition, but the patient was not psychically suitable for thorough measures.

The treatment cannot be considered ideal in view of the dietary irregularities
and excesses. It represents undernutrition to the extent of reducing the body
weight from 53.6 kg. on admission to 47.6 kg. on discharge; i.e., a loss of 6 kg.
As a result the patient felt stronger and more comfortable, and was free not only
from the urinary signs of diabetes but also from his former subjective symptoms.
The marked neurasthenia remained. The outcome is satisfactory to the extent
that the patient was kept in a tolerable condition for S| months in hospital and
was symptom-free at the close, while the actual severity of his condition was
demonstrated by death after 2 months of unregulated diet following discharge.

CASE NO. 10.

Male, unmarried, age 17 yrs. Irish American; plumber. Admitted Nov. 7,
1914.

Family History. — Grandparents lived to old age. Parents living and well.
One brother died in infancy; one brother and three sisters living and well. No
diabetes or other disease known in family.

Past History. — Healthy, vigorous life. Measles and whooping-cough in child-
hood. No other infections; no venereal disease, alcohol, or tobacco. Has
worked hard as plumber's helper since stopping school at 14, but he was strong
and the work was no strain on him. Always a heavy eater; partiailarly candy,
ice cream, pastry, and everything sweet taken in large quantities. Normal
weight 133 pounds.

Present Illness. — Last Jan. or Feb. the patient began to drink two gallons of
water per day and pass urine correspondingly. He felt well at this time and was

CASE RECORDS 225

1000 calories was made on Dec. 29. Jan. 5 was a complete fast-day, Jan. 26 an-
other. Generally reduced diet was used instead of fast-days because of the pa-
tient's weakness. He gained strength very markedly during the course of treat-
ment and began to look and act almost like a well boy. Exercise was employed
with apparently great benefit, especially as he was naturally strong and muscular.
He walked many miles daily, went skating on the ice, and undertook other
activities.

Toward the close of Jan. he and his parents considered that a cure had been
achieved and that he was ready to go to work. As long as he felt ill he was an
ideal patient. At this time, feeling well, he began to rebel at diet and all other
hospital rules. The glycosuria and ketonuria during and just preceding the
month of Feb. are attributable not to the prescribed diet, but to violations on the
part of the patient. It became necessary to discharge him on Feb. 8, and he was
informed that in view of his conduct this hospital could have no further connec-
tion with his case. It was learned that he followed no regular diet thereafter, and
died Mar. 9 with the usual acidosis symptoms.

Acidosis. — The only alkali given was 10 gm. sodium bicarbonate on Nov. 11.
In the absence of alkali treatment the excretion of acetone bodies was relatively
low, reaching only 13.2 gm. of /S-oxybutyric acid on Nov. 10. For the same
reason the ammonia excretion was high in comparison, being 3.4 gm. on Nov.
10, 4.75 on Nov. 11, and 4.46 on Nov. 12. It is evident that fasting with alcohol
did not immediately bring about a low ammonia, but beginning Nov. 12 the
steepest fall occurred, down to 1 .5 gm. on Nov. IS, and 0.42 gm. on Nov. 20. The
clinical symptoms cleared up much more strikingly than the ammonia.

On the too abundant carbohydrate-free diet of Dec, the ammonia never fell to
a normal level. It seemed to rise quite markedly after stopping alcohol on Dec.
16, so that on Dec. 22 and 26 it was slightly above the level of Nov. 14 (2.18 gm.).
Dec. 27, with a diet solely of whisky representing 85 gm. alcohol, brought a strik-
ing drop in the ammonia, and on the lower diet following this date the ammonia
never returned to the height of this peak, but also did not fall to normal. It
could presumably have been brought down to normal by the use of alkali, but the
advisability of alkali for this purpose under the circumstances is open to question.
In this same period the ferric chloride reaction was entirely negative. Alkali
would presumably have made it positive and increased the excretion of total
acetone bodies. The desirability of this change is also an unknown matter. The
real trouble was an unsuitable diet.

Blood Sugar. — The accuracy of the single determination showing an unexpect-
edly low blood sugar on Nov. 13 is doubtful. While irregularities are possible, it
seems more probable that the blood sugar remained close to 0.25 per cent until
about the close of the fast and then it fell to below 0.15 per cent. The occasional
analyses up to Dec. 15 showed a tendency to remain within normal limits. Fur-
ther analyses were not possible at the time. More attention should have been
paid to this point. In correspondence with the improvement otherwise, it would

226 CHAPTER in

seem that the case was still at a stage when normal blood sugar values were rather
easily attainable, and such should have been insisted upon.

Remarks. — The earlier part of the treatment was well carried out, and the
patient, threatened with coma, was rapidly freed from ketonuria, glycosuria, and
hyperglycemia. This was still at an early period of experience with this method;
it had not yet been learned that apparent restoration of tolerance is not to be
trusted too far, and that weakened function does not so rapidly recover to this
extent, but that it must be continuously spared by prolonged undernutrition.
Therefore, a carbohydrate-free diet was built up too fast and too high. Even in
the absence of laboratory danger signs, it is now known that such a procedure
inevitably brings disaster later. The lower diet of early Jan. was more rational.
But in general, instead of trying to make the patient feel too well and build him
up too rapidly, a more stringent limitation of both diet and weight should have
been insisted upon. The patient was received weighing 41.6 kg. After a sharp
initial drop to 39 kg. in the early days of fasting, the weight remained stationary,
then rose sharply as a result of water retention. Even with the weight of 45.6
kg. on Nov. 28 he did not appear edematous. His tissues had evidently been
dried before and retained water subsequently, so that he looked and felt better.
The water thus stored on undernutrition was then driven out by increase of the
carbohydrate-free diet, probably especially by the increase of fat, so that by
Dec. 15 weight had fallen to the same level as at entrance. Nevertheless, the
period from Nov. 28 to Dec. 15 must be regarded as one of actual gain of body
substance. There was some perceptible edema when the weight rose above 47
or 48 kg., as on Dec. 22 and Jan. 4. The patient was discharged weighing 45 kg.,
and at least part of the gain over the entrance weight may be regarded as actual
increase of body tissue. This gain should be considered as harmful not only in-
directly, owing to the fact that the patient became too confident from feeling too
well, but also directly, inasmuch as tolerance ought to have been built up in-
stead of weight. Trouble would have resulted later from this condition even if
the patient had remained faithful, and it would have been necessary to make a
radical restriction of his diet. Also the therapeutic possibilities are never so good
after several months of imperfect treatment as at the outset. The cause of the
final disaster was, however, the deep ignorance and lack of education of the
patient and his entire family, who had no conception of the nature of the disease
and were deaf to all advice as soon as the patient felt fairly well. Under such
circumstances a successful outcome was precluded. The favorable side of the
case is that such a degree of well-being and freedom from symptoms was attained
during the 3 months in hospital, while the severity of the case was demonstrated
by the death in comal month after breaking diet.

CASE RECORDS 227

CASE NO. 11.

Female, married, age 55 yrs. Austrian; housewife. Admitted Nov. 9, 1914.

Family History. — Father died at 55, cause unknown. Mother died at 70.
Three brothers and three sisters of patient were healthy; one of them died at 65.
Family are obese. No diabetes or other family disease known.

Past History. — Patient has been strong and weU, though obese. As a young
woman she weighed over 200 pounds, more recently she has considered 183 pounds
her regular weight. No infections, except measles at 16. No sore throats.
She was married at 21 ; four miscarriages; nine children born alive, four of whom
died in infancy. All of those alive are more or less obese.

Present Illness. — 10 years ago she began to notice a bitter taste after eating,
also constipation. 7 years ago a doctor found 7 per cent sugar in the urine, and
by dieting reduced it to 2 per cent. She had followed prescribed diets during
these 7 years, but sugar was never below 2 or 3 per cent. She thinks she has lost
weight chiefly in the last few weeks. She continued to do housework until last
week, when she went into collapse, pale, exhausted, and vomiting blood. Her
physician reported 7 per cent sugar in the urine. He prescribed a diet of noth-
ing but green vegetables for 3 days. Vomiting then made eating impossible.
Patient entered hospital in this condition with extreme weakness, anorexia and
nausea, pain in chest and abdomen, hemoptysis, headache, and dyspnea. The
blood brought up at first is described as being brighter and more abundant than
now.

Physical Examination. — An obese woman with appearance of prostration, face
pale, also extremely cyanosed, cyanosis extending into neck. Moderate constant
dyspnea, a weak frequent cough bringing up sputum either bloody throughout or
streaked with dark blood. Slight jaundice. Lungs: resonance, passing into
dulness at bases, especially posteriorly; breath sounds become bronchial in
character over dull areas and are everywhere rough. Coarse, loud riles every-
where. Heart is enlarged to 16 cm. to left of midsternal line and other signs are
those of mitral regurgitation. Liver is easily palpable, lower border extending
from 2 cm. below umbilicus obliquely into right flank barely above iliac crest.
Pain and tenderness complained of over liver, also pain down left arm. Leg
veins badly varicosed. Examination otherwise negative.

Treatment. — The patient necessarily remained in bed and was treated by the
cardiac service of the hospital with digipuratum for her evident heart failure. The
temperature ranged from 37 to 37.6°, the pulse from 92 to 112. The urine was
strongly acid, with specific gravity 1020 to 1025 and considerable albumin. The
general clinical record is given in Table VHI.

The patient was both weak and drowsy, and the symptoms were evidently due
to a combination of acidosis and heart failure. She took no food on Nov. 9 and
10, nevertheless glycosuria was heavy and weakness seemed to be critical. The
condition had arisen on a diet limited to green vegetables, and the consequences

CASE RECORDS 229

Present Illness. — About 3 years ago abnormal weakness, thirst, and polyuria
appeared. A physician found glycosuria of 7 J per cent. He ordered abstinence
from sugar and pastry. The glycosuria thus diminished to 2 per cent and the
patient felt fairly well, but after 8 months on the same diet the sugar rose to 5i
per cent and weakness returned. He has been unable to work for the past 2
years. For the past week he has been confined to bed because of weakness and
pains in chest and back. There has been cough, especially at night for 2 months
past. No fever and no hemoptysis now, but there was spitting of blood on three
occasions last winter. 18 months ago small ulcers appeared on both feet and
have slowly extended instead of healing; they are painful only when he walks.
He is now nervous and constipated, and teeth have decayed rapidly. He has
continued to lose weight.

Physical Examination. — Patient stiU appears comfortably nourished, with good
color in face. Tonsils slightly enlarged; part of left one is missing. Viscera
no^al to examination. Blood pressure 150 systolic, 95 diastolic. A few patches
of lichen planus on arms. Legs show small varicose veins threatening to ulcerate
at some points. The skin is pigmented and scaly, somewhat eczematous. Sev-
eral small superficial ulcers are present on ankles and feet. No gangrene. Strong
pulse in dorsalis pedis arteries.

Treatment. — Supper was given on the day of admission and then fasting imme-
diately begun. Though glycosuria cleared up in 2 days, the patient being over
weight was given 4 days of absolute fasting followed by 2 alcohol days, then 4
days of green vegetables, then 3 fast-days, and then a diet of moderate undernu-
trition. The superficial infections cleared up promptly. It is a question whether
the trace of glycosuria on Nov. 16 on taking 220 cc. whisky was attributable to
the alcohol. As frequently found at the outset in cases of this type, the food toler-
ance was rather low. Early in Dec. a diet with only 10 gm. or less of carbohy-
drate caused occasional traces of glycosuria, and in the period Dec. 17 to 25 the
attempt to give IS to 40 gm. carbohydrate had to be abandoned because of per-
sistent glycosuria. At the same time the total diet, if the mean body weight be
taken as 80 kg., represented approximately 1 gm. protein and only 25 calories per kg.
On strictly carbohydrate-free diet the patient proved able by Jan. 7 to 8 to take
116 gm. protein and 2600 calories without glycosuria. As he had now been re-
duced by about 11 kg., it was considered advisable in view of his age to allow a
diet of this sort and let him have the benefit of improved living conditions in the
Country and such exercise as he might be able to take. He was therefore dis-
charged on Jan. 9 with this purpose in view.

Subsequent History. — The patient reported at intervals that he was free from
glycosuria, and occasional examinations at the hospital showed absence of sugar,
very slight ferric chloride reaction, and a tendency to gain weight on the pre-
scribed diet. Though he looked well he complained of continual weakness which
made him unable to work. He was very faithful to all instructions, and when
unable because of poverty to obtain the prescribed food he fasted altogether.
He was readmitted to the hospital May 5 for further treatment.

230 CHAPTER m

Second Admission. — The weight at this admission was 82.6 kg.; i.e., about 4
kg. less than at his former admission and about 7 kg. more than at his former
discharge. His food tolerance appeared perceptibly higher, as he was now able
to take a diet of some 120 gm. protein, 50 gm. carbohydrate, and 3000 calories
without glycosuria. On account of the weekly fast-days these figures must be
reduced by ^ to give the actual average intake. Undernutrition was shown by
the fall in weight during stay in hospital. The weight gained outside of hospital
was evidently due to unintentional overstepping of the prescribed quantities. Two
determinations of the blood sugar gave values below 0.15 per cent. A fairly lib-
eral diet was permitted with a view to overcoming the marked weakness, and
exercise within the patient's limited capacity was also encouraged for this pur-
pose. Shortly before his second dismissal he was made accustomed to a diet of
about 100 gm. protein, 50 gm. carbohydrate, and 2500 calories, which repre-
sented a reduction below his known tolerance to allow for unintentional errors.
He was dismissed on June 29 greatly improved in all respects, and was advised
again to take a rest in the country for general hygienic reasons.

Subsequent History. — He reported in person on Sept. 7 with normal urine, feel-
ing able to do moderate work. On Nov. 29 he was seen again; sugar and ferric
chloride reactions were regularly negative and he was making his living at his
usual work. He had gained about 2 kg. since discharge. The same condition
has continued with steady improvement up to the present. He now feels well
constantly and carries on his work without difficulty. His diet satisfies him and
urine remains normal.

Remarks. — This case is a good illustration of a numerous type — diabetes rela-
tively mild but finally bringing the patient to a state of disability. The clearing
up of such a condition generally proves to be neither quick nor easy. The most
important therapeutic measure is the reduction of weight, which, however, may
not have to be carried to the point of emaciation. The patient is benefited
slowly. Unless he has full confidence in the physician, he is likely to abandon
treatment because of the tedious privations of diet and the apparent lack of
benefit. At first he sometimes even looks and feels worse than before.

For the sake of strength, liberties were taken here in the direction of high
feeding which would have meant disaster to a younger patient. More protein
and less fat would doubtless have been better. With a weak patient at such an
age, it was considered that the slight persistent ferric chloride reactions could be
temporarily ignored. The outcome justified the procedure, since the continued
freedom from glycosuria finally brought with it freedom also from ketonuria; but
probably results could have been obtained still more rapidly by taking account
of the acidosis and giving fairly Kberal protein for the sake of strength, very little
fat, in order that the patient might burn off his own fat, and a little carbohydrate
if possible. The salvation of this patient lay in his absolute fidelity. He occa-
sionally imderwent serious privations on account of poverty without once being
tempted to take forbidden food. His age is clearly a factor in the favorable out-

CASE RECORDS 231

come. He shows a tendency to gain tolerance with time. He is able to keep
on a normal level of nutrition, and is not impaired in comfort or usefulness at
present by his diabetes.

CASE NO. 13.

Female, age 11 yrs. American; schoolgirl. Admitted Nov. 14, 1914.

Family History. — Paternal grandfather died of cancer. Antecedents otherwise
healthy. Parents healthy. Five brothers and sisters of patient healthy. No
obesity or other abnormalities.

Past History. — Patient always well, apparently the strongest of the six children.
Whooping-cough and measles before 5, mumps at 6, all mild without sequelae.
Adenoids removed at 6. No sore throats. Regular life, not nervous. Candy
and sweets taken in very limited quantity. Appetite, bowels, sleep, normal.
Highest weight 59 pounds in 1913.

Present Illness. — Sugar was found in urine April 21, 1914, the reason for medical
examination being only slight languor for a very few days preceding. Weight at
this time 57 pounds. She was placed immediately on the usual carbohydrate-free
diet, with gluten bread and occasionally a little ordinary bread, a quart of milk
every day, and a little oatmeal gruel. For the past 6 weeks the quantity of
oatmeal has been increased. Butter and cream were used as liberally as possible
and egg-nogs were given between meals. On this maximum caloric diet she steadily
lost weight. Weight 1 week ago 52J pounds. She was given Fowler's solution
of arsenic sometimes. Sodium bicarbonate was given to the extent of J teaspoon-
ful three times a day for a few days several weeks ago, but was stopped because
it seemed to upset the stomach. For 2 weeks past the increased respiration of the
child had attracted the attention of her attendants, but she still seemed cheerful
and alert. Hair falling out rapidly for past few weeks, ififowels constipated.

Physical Examination. — A fairly normal looking, though thin little girl, lying
quietly in bed with noticeable but not extreme polypnea. Cheeks are flushed
more than normal. Teeth in good condition. Both tonsUs moderately en-
larged. No lymph gland enlargement. Blood pressure 105 systolic, 75 diastolic.
General dryness of skin, most marked on legs. Examination otherwise negative.

Treatment. — The patient received a moderately restricted diet of 1000 calories
for 1 full day in hospital (Nov. 15) when, with 46 gm. protein and 57 gm. carbo-
hydrate in the diet, she excreted 46.8 gm. sugar. Fasting was then begun with
about 20 cc. of whisky daUy. Glycosuria ceased after 3 days of fasting. On
Nov. 19 green vegetables were added to the extent of 3 gm. carbohydrate, and
4 gm. on Dec. 20 and 21. The glycosuria of Dec. 20 seemed to be
clearly due to this quantity of carbohydrate, since violations of diet were posi-
tively excluded. It cleared up spontaneously the next day, as this sort of glyco-
suria often does. On Nov. 22, 40 gm. sugar-free caramel were given'' in doses of

* 40 gm. caramel given on Dec. 29 not shown in graphic chart.

232 CHAPTER ni

5 to 15 gm. throughout the day. No glycosuria resulted, though the tolerance
was so low. As the patient needed a diet to conserve strength, the food on Nov.
23 consisted of 3 eggs and 14 gm. alcohol. Nov. 24, SO gm. steak were added.
Nov. 25, the meat was increased to 100 gm. On the following days fat was added
in the form of bacon and oUve oil, so that on Nov. 29 to 30 the diet was approxi-
mately 46 gm. protein and 1100 calories, or 2 gm. protein and 50 calories per kg.
for a weight of 22 kg. This allowance, abundant even for a child, caused glyco-
suria. It was checked by a sharp reduction of diet. The glycosuria shown at
intervals during the next 3 months was always slight, generally no more than
faint traces in certain periods of the day, often indistinguishable if the tests were
performed upon the mixed 24 hour urine, and sometimes connected with urinary
calculi or with the .use of vegetables.

! The condition was compUcated by the former trouble. In Dec, the patient
complained of pain in back and bladder region, and painful urination. Later
^loody urine was passed and some small clots. On Dec. 21, examination was
piade by a urologist, and the next day x-ray plates were taken. Nothing posi-
tive was found, but on subsequent days a few tiny calculi were passed. Several
milder attacks of this character occurred subsequently, and seemed in each
instance to aggravate slightly the tendency to glycosuria.

The diet was carbohydrate-free in the strictest sense, inasmuch as this pa-
tient could not tolerate thrice cooked vegetables, but showed glycosuria when
attempts were made to use them. For example, on Jan. 23, after 2 weeks of
complete sugar-freedom, 250 gm. thrice cooked celery were added to the diet and
glycosuria appeared. The vegetables were stopped and the diet reduced, and the
glycosuria ended. Then, on Jan. 25, 100 gm. each of thrice cooked celery, as-
paragus, and Brussels sprouts were added, and on Jan. 26, 100 gm. each of the
asparagus and Brussels sprouts without celery. The sUght glycosuria was checked
by a fast-day with 11 gm. alcohol on Jan. 28. On Jan. 29 the attempt to use 300
gm. thrice cooked vegetables was resumed, and it was again necessary to stop
glycosuria by a fast-day on Feb. 1. Traces of glycosuria then reappeared when
diet was resumed without the vegetables, indicating that some injury had been
done, but a glance at the graphic chart will show that the patient soon was able
to take a higher diet without glycosuria when all vegetables were omitted (e.g.
45 gm. protein and 670 calories on Jan. 23, with vegetables, with glycosuria;
45 gm. protein and 850 calories on Feb. 26, without vegetables, without glyco-
suria). The abiUty to tolerate higher diets during the first half of Apr. (up to
63 gm. protein and over 1900 calories on Apr. 17) must be attributed to a gradual
gain in tolerance. Improvement was finally indicated by the ability to remain
sugar-free on decidedly higher diets.

As the home conditions were good and the parents absolutely trustworthy,
it was considered feasible to let the patient take a vacation at this critical period
in her treatment, for relief from the abnormal hospital environment. She was
therefore dismissed on June 5 with the idea that she might be able to spend
perhaps 2 or 3 weeks at home.

CASE RECORDS 233

Acidosis. — This was first measured by analyses of the acetone bodies and am-
monia. At the outset, the characteristics of acidosis without alkali treatment
were seen in the moderate ketonuria and high ammonia. Beginning Nov. IS,
20 gm. each of sodium bicarbonate and calcium carbonate were given daUy. The
sodium bicarbonate was stopped on Nov. 25, but the calcium carbonate continued
until Dec. 4. The beginning of protein-fat diet on Nov. 23 caused a rise of the
ammonia from 0.45 gm. up to 0.98 gm. notwithstanding the use of alkali. The
stopping of sodium bicarbonate on Nov. 25 brought an immediate jump of the
ammonia up to 1.8 gm. Seemingly the continuance of 20 gn^ calcium carbonate
daily did not serve to prevent this high ammonia. Also as usual the bicarbonate
apparently served to keep up the ferric chloride reaction, for this quickly became
pale after bicarbonate was discontinued. It is seen that the ammonia gradually
fell to a level which may probably be considered normal on protein-fat diet, also
the ferric chloride reaction became negative, not in consequence of the use of
carbohydrate which was formerly considered necessary to combat diabetic acidosis,
but solely by reason of the gradual undernutrition. Determinations of the blood
alkalinity were begun on Jan. 29 and showed a subnormal level of 47 vol. per cent.
On Feb. 6, the level was still lower, viz. 41 per cent, and on Feb. 13 a still lower
value of 39.5 per cent was found. The condition took care of itself without the-
use of any alkali, and the combining power of the plasma remained at or above 50
vol. per cent until the close of Apr. Up to this point the ammonia excretion and
the ferric chloride reaction proved the more sensitive indicators. It wiU be noted that
the ammonia curve touched its lowest point at practically the identical time with the
lowest point of the weight curve, namely the middle of Feb., and the ferric
chloride reaction was negative at the same time. With the increase of protein-
fat diet came a gradual and practically parallel rise of the ammonia and weight
curves; also ferric chloride reactions appeared and increased correspondingly.
In the fasting periods, Apr. 29 to May 1 and May 16 to 18, the plasma bicarbon-
ate gave indications of acidosis not revealed by the other tests. The ferric
chloride reaction was not perceptibly altered, and the ammonia excretion distinctly
fell in both fasts. The lowering of the plasma bicarbonate may serve as a delicate
indicator under such circumstances, since it sometimes falls to a point giving
warning of dangerous acidosis in fasting, and at this point clinical symptoms
correspond. The degree of the fall was not dangerous here, and chnical symp-
toms were absent. In the period May 15 to 19 inclusive, 5 gm. sodium bicarbon-
ate were given daily with 30 cc. whisky, to test whether this combination of alkali
and alcohol had any effect upon the fasting acidosis. The result showed only a
slight difference as compared with the period Apr. 29 to May 1. The ferric chlor-
ide reaction was unchanged, the ammonia was a bare trifle lower and the plasma
bicarbonate a trifle higher, but the difference was within the range of accidental
variation. Carbohydrate from 10 to 30 gm. in the forepart of May faUed to
clear up the ferric chloride reaction, which also persisted through fasting, but be-
came negative on the fast-day of May 23 and remained so until the diet was m--

234 CHAPTER ni

creased on June 2. Here it is evident that simple increase of fat produced this
reaction.

Blood Sugar. — ^This was determined only occasionally in the period Apr. 16 to
May 21, samples being taken in the morning before breakfast. The first two de-
terminations were approximately 0.15 per cent. This was considered too high,
and the period of almost 4 days of fasting (Apr. 28 to May 1 inclusive) was im-
posed for the purpose of bringing it down. It was thus made and kept normal
(as far as fasting values were concerned) until the increase of carbohydrate
to 30 gm. on May 14 brought glycosuria with hyperglycemia of 0.18 per cent the
fofllowing morning. A similar fasting period then succeeded in bringing it down
almost to normal. The alkali given as above described during this phase did
not serve to bring the blood sugar lower. Hyperglycemia again resulted from the
subsequent diet containing 10 gm. carbohydrate, and this was one of the reasons
for omitting this carbohydrate.

Weight and Nutrition. — In the period Nov. 16 to 22 inclusive, with practically
no nitrogen intake, there was a loss of 20.55 gm. nitrogen in the urine. In the
first 3 months in hospital, undernutrition is indicated by the fall in weight from
21,2 kg. on Nov. 16 to 16.8 kg. on Feb. 16, being a loss of 4.4 kg., or about one-
fifth of the weight at entrance. The diet of this period, after the brief excess in
Nov., was in the neighborhood of 45 gm. protein and 700 calories, or a little
over 1 gm. protein and 35 calories per kg. of weight, but the rather frequent
days of fasting or low diet reduced the average materially below this figure. Gain
in weight began with the increase of diet in the latter part of Feb. In conse-
quence, both sugar and ferric chloride reactions were present early in Mar. There-
after the ferric chloride tests and the unduly high ammonia were the chief indi-
cations of improper diet.

In the early half of Apr. the ration was generally 63 gm. protein and 1700 to
1900 calories (about 3.3 gm. protein and 90 to 100 calories per kg.) with fast-
days somewhat reducing this average. On Apr. 19 a better balanced diet was
instituted, consisting of 49 gm. protein, 5 gm. carbohydrate, and 1322 calories,
increased by May 14 to 57 gm. protein, 30 gm. carbohydrate, and 1593 calories.
Distinct glycosuria resulted at this time. After a period of fasting, a decidedly
lower diet was given beginning May 19. Though the ability had been shown to
tolerate 10 gm. carbohydrate during this time, it was considered safer to boil out
carbohydrate in the diet at home. Accordingly the diet prescribed at discharge
consisted of 68.5 gm. protein, 250 gm. thrice cooked vegetables, and 1500 to 1600
calories (about 3.5 gm. protein and 80 calories per kg., reduced by weekly fast-
days to about 3 gm. protein and 70 calories average).

At discharge the weight was 19 kg.; i.e., 2.2 kg. less than at admission. The
half year of treatment thus represented imdernutrition to this extent. There
was no gain, and if anything a slight loss of strength, also no growth in stature.
The child was thoroughly cheerful, and able to be about and keep herself amused
all day.

CASE RECORDS 235

Subsequent History.— The progress at home was better than expected. Reports
and samples of urine showed continued absence of both sugar and ferric chloride
reactions. On July 1 the addition of 5 gm. carbohydrate was tolerated. On Aug.
1 an increase to 10 gm. carbohydrate brought a trace of glycosuria. The allow-
ance of S gm. continued to be tolerated, and the child gained also in weight and
appearance. Oct. 3, occasional traces of sugar were reported, and on advice the
patient returned to the hospital on Oct. IS for further treatment, having suc-
ceeded in remaining in good condition at home for 4 months instead of the few
weeks anticipated.

Second Admission. — The patient returned weighing 20.8 kg.; i.e., with a gain of
1.9 kg. over her weight at discharge and a loss of O.S kg. from her weight on first
admission. Her appearance and actions indicated a decided gain in vigor.
On the same carbohydrate-free diet prescribed at discharge she showed moderate
glycosuria, marked hyperglycemia (plasma sugar 0.25 per cent), a well marked
ferric chloride reaction, and a slightly subnormal plasma alkalinity. Accordingly
fasting was begun on Oct. 17, and sugar-freedom resulted within the first 24 hours.
After an additional 24 hours of fasting, a carbohydrate tolerance test with green
vegetables was begun for the usual diagnostic and therapeutic reasons. Beginning
as usual with 10 gm. carbohydrate on Oct. 19, an increase of 10 gm. carbohydrate
was made daily, with the result that 60 gm. carbohydrate was established as the
tolerance. The traces of glycosuria on Oct. 25 and 26 exemplified the false limit
sometimes encountered in such tests, when there is a trivial excretion on a cer-
tain intake, which disappears after this intake is continued or increased. This
affords no comparison with the tolerance on the previous admission, because no
test was then made with carbohydrate in the absence of other foods. In con-
sequence of this undernutrition with carbohydrate to the point of tolerance, the
blood sugar as determined mornings before breakfast fell to normal, the ferric
chloride reaction became negative, and the plasma bicarbonate rose to normal.
After a fast-day on Oct. 31 to clear up the glycosuria resulting from the carbo-
hydrate test, a diet was begun which was better planned than on the previous
admission; namely, 50 gm. protein, 10 gm. carbohydrate, and 1000 calories. Be-
cause of glycosuria it was necessary on Nov. 8 to reduce the carbohydrate, and
after Nov. 15 it was regularly 5 gm. For a body weight of 20 kg., this diet rep-
resented 2.5 gm. protein and 50 calories per kg. The weekly fast-days reduced
this to an average of approximately 2.14 gm. protein and 43 calories per kg.
The general well-being was definitely improved by this lower diet and the intro-
duction of carbohydrate, as compared with what was observed on the previous
admission. The carbon dioxide capacity of the plasma, which had been as low
as 45 per cent, rose to 55 per cent without the use of alkali. The blood sugar,
which had risen with the appearance of glycosuria at the close of the carbohydrate
test, continued unduly high, but remained below 0.2 per cent and gradually fell
below 0.15 per cent. The patient was dismissed on Dec. 14 weighing 19.3 kg.;
i.e., 1.5 kg. below her weight at this admission, and 0.4 kg. above her weight at
the former discharge.

236 CHAPTER III

Exercise. — During the former time in hospital the chUd was kept at rest, partly
because of weakness. This time she was given regular exercise to the limit of
comfortable endurance. No detailed studies were made, but it was evident that
no striking increase in tolerance was produced in such a severe case of diabetes.
Existing glycosuria was not cleared up by exercise, also it was not possible to
raise the carbohydrate ration higher with exercise than without. On the other
hand, the exercise certainly did no harm; it may have had a share in the gradual
reduction of the hyperglycertua; and it unmistakably improved the strength, well-
being, and enjoyment of the child. The exercise was mostly in the form of ball-
tossing, walking, roUer-skating, and other play.

Subsequent History. — The patient remained sugar-free at home, and took up
some school work in Feb., 1916. Increase of carbohydrate to 10 gm. was tolerated
without glycosuria. In May she caught cold, showed traces of sugar almost con-
stantly, and lost IJ pounds in 2 weeks by reason of the undernutrition necessary
to keep down glycosuria. Her former tolerance returned with recovery ftom the
cold. Glycosuria remained absent practically continuously until July, when
persistent traces of sugar made it advisable for the patient to return to the
hospital.

Third Admission. — ^July 7, 1916. The weight at this admission was 20 kg.;
i.e., 0.7 kg. more than at discharge 6i months previously. The height was 132
cm. Under regular diet, July 7 to 10 inclusive, there were stiU marked sugar and
ferric chloride reactions. The plasma sugar on July 11 was again 0.25 per cent,
and a rigid period of undernutrition, including fasting and a carbohydrate test,
was therefore instituted. The tolerance for carbohydrate was identical with
that in the previous October. The treatment reduced the blood sugar to 0.13
per cent, but it rose to 0.22 per cent on resumption of the previous diet. The
weight was thereby reduced to 17.2 kg., which was lower by 4 kg. than at the
first admission. The patient was still cheerful and active, and returned home in
this condition.

Subsequent History. — In Aug., on account of shght glycosuria, carbohydrate was
omitted from the diet. The disturbance seemed to be associated with kidigestion.
Otherwise the sugar and ferric chloride reactions remained negative. The patient
attended school half of each day, and took automobile rides and other recreation.
In Oct. bloody urine reappeared and two small calculi were passed. This trouble
seemed to affect her diabetes very badly, and for this reason she reentered the
hospital Oct. 24, 1916.

Fourth Admission. — Weight 19.3 kg. Appearance thinner, paler, and weaker
than previously. The change for the worse is said to date from the attack of cal-
culi. The urine by this time was free from blood, and physical and x-ray examina-
tions were negative. The patient was made sugar-free by 2 days of fasting, then
given green vegetables representing S gm. carbohydrate the first day, increasing
by 5 gm., daily up to SO gm., which was the Umit of tolerance; i.e., a loss of 10 gm.
as compared with previous tests. She was then placed on a diet of 30 gm. pro-

CASE EECOIOJS 237

tein, 20 gm. carbohydrate, and 600 calories, and was encouraged to exercise
within the hmits of her strength. A routine fast-day was given once a week.
Because the strength remained low, this diet was changed on Nov. 23 by dimin-
ishing the carbohydrate to 10 gm. and increasing the protein to 40 gm. For the
same reason on Dec. 4 carbohydrate was omitted from the diet and the protein
increased to 45 gm. The patient at this time took walks of 8 blocks without
weariness, and was outdoors much of each day. Blaud's pills were given because
of anemia. The patient remained in hospital until Feb. 1, 1917, when she was
dismissed on a carbohydrate-free diet of 40 gm. protein and 700 calories, weigh-
ing 17 kg.; i.e., 1.2 kg. less than at this admission, and 4.3 kg. less than at her
original admission in Nov., 1914.

Acidosis. — The ferric chloride reaction remained constantly negative. Traces
of acetone were constantly present, as must be expected on such a diet. There
was a daily excretion of 0.18 to 0.64 gm. ammonia nitrogen, the output being
lower in the earUer period of lower calories with carbohydrate in the diet. Symp-
toms of acidosis were entirely absent, and the carbon dioxide capacity of the
plasma was 65.3 per cent at dismissal.

Blood Sugar. — ^Hyperglycemia was continuous, in general close to the threshold
of glycosuria as shown in the charts of former periods. The blood sugar at dis-
missal was 0.2 per cent.

Subsequent History. — The condition continued the same at home as in hospital,
the patient remaining very thin but bright and active. In Mar. a "green day"
was advised in the middle of each week to break the monotony of the diet, di-
minish the total calories, and introduce carbohydrate. Traces of sugar appeared
only occasionally and at first cleared up with the routine fast-days. The usual
slow downward progress occurred under these circumstances, but owing to the
■derangement of the hospital organization by the military emergency, the patient
was not required to return for treatment until Oct. 10, 1917. By this time she
had been seriously weakened by the frequent fasting necessary to control glyco-
suria, though she was still up and about.

Fifth Admission.— Oct. 10, 1917. Weight 16.6 kg. The patient had stood the
trip from Massachusetts very well. One day of fasting cleared up the shght
existing glycosuria. On the second fast-day the plasma sugar was 0.098 per cent,
CO2 capacity 55 per cent. On the evening of the second day the fast was broken
with 5 gm. carbohydrate in the form of a salad. The urine was continuously nega-
tive for both ferric chloride and nitroprusside reactions, and the nitroprusside test
of the plasma was likewise negative. Carbohydrate was increased by 5 gm. daily
without glycosuria. Oct. 16, breakfast was taken as usual, but collapse occurred
about 10 a. m. and death about noon, preceded by slight tetanoid convulsions.
The urine at this time was still normal. The blood showed hemoglobin 22 per
cent, plasma sugar 0.02 per cent, CO2 capacity 69.7 per cent. The employment
of the carbohydrate test was a mistake, for though the child was up and about
until the day before death, the low blood sugar on the second fast-day was a

238 CHAPTER in

pkin indication of exhaustion, and protein should have been fed instead of car-
bohydrate. Nothing, however, could long have prevented the fatal termination
under the circumstances at this time.

Remarks.— The patient presented juvenile diabetes of great severity. Within
about half a year she had come close to coma and had lost carbohydrate tolerance
almost completely. It is evident that the assimilation had already fallen too low
to support growth, owing to lack of treatment in the earlier stage. Under treat-
ment she was then kept alive and in tolerable comfort and activity for nearly 3
years. Two aspects of the progress may be noted.

On the one hand, no special tendency to recovery of assimilative function has
been manifest. During the first period of over 6 months in hospital, it is true
that the food tolerance decidedly improved, but this result was merely the accom-
paniment of some 2 kg. loss of weight and does not necessarily indicate any
change in the fundamental assimilative power. At the second admission the
weight was up almost to the original figure, but other conditions were different.
Active diabetes was present again at this admission. The carbohydrate tolerance-
was tested with exclusion of other foods. Thereafter carbohydrate could be in-
cluded in the diet, but this was on a lower ration than during the first admission.
Real improvement in assimilation would have meant that the child could grow in
weight and stature; on the contrary, the third and fourth admissions represented
further loss of weight. The carbohydrate tolerance in July, 1916, was the same
as in Oct., 1915, but as the latter test was at a lower body weight, the result may
be interpreted as actual downward progress.

On the other hand, the record furnishes evidence against the "spontaneous"
character of such downward progress. Hyperglycemia was almost continuous,,
and glycosuria and ketonuria recurred rather frequently throughout the entire 3
years. A partially depancreatized dog under similar conditions would have gone
into hopeless diabetes much sooner. Any inherent downward tendency should
have been perceptible in this type of case in this length of time. The slow change
observed is abundantly explainable by the prolonged slight overstrain of the
weakened function.

CASE NO. 14.

Male, married, age 51 yrs. American; optician. Admitted Nov. 16, 1914.

Family History.— Fkthei died of typhoid at 28, mother of heart trouble and'
dropsy at 55. Two sisters living and well. Patient has been married 23 years;
one child dead, one living and well. Tuberculosis, cancer, syphilis, diabetes, and
other family diseases denied.

Past History.— Kenlthy life. Scarlet fever in childhood. Occasional sore
throats. Gonorrhea twice. Syphilis denied by name and symptoms. In Apr.,
1914, he was confined to bed with so called dry pleurisy and had cough and
slightly blood-tinged expectoration for 3 or 4 weeks. Constipation, slight indi-
gestion, moderate or poor appetite. Alcohol used rather freely but not to-
drunkenness. Moderate tobacco.

CASE RECORDS 239

Present Illness. — 7 years ago patient states that he strained himself lifting a
trunk. He had pain in the back for several months, therefore had his urine
examined and sugar was found. He claims never to have had any of the typical
diabetic symptoms. He now complains of indefinite neuritic pains in back and
legs. His best weight was 140 pounds 6 years ago; now 112. A few days after
• admission the patient's wife volunteered the information that he had undertaken
a number of different treatments for his diabetes at different times, but had never
adhered to any prescribed diet for even a brief time.

Physical Examination. — ^A fairly developed, poorly nourished man. Teeth
mostly absent, little decay in those remaining, slight pyorrhea. Throat con-
gested but tonsils not visibly enlarged. Cervical, axiUary, epitrochlear, and in-
guinal glands slightly enlarged. Reflexes very active. Blood pressure 100 sys-
tolic, 70 diastolic.

Treatment. — ^After 2 days of observation on a low protein-fat diet, fasting was
begun on Nov. 18. On Nov. 20 to 22 he received 27 to 35 gm. alcohol. This
S day fast greatly diminished but did not quite abolish glycosuria. The ferric
chloride reaction, which was negative on the day of admission, became strongly
positive on the carbohydrate-free diet and on fasting. The weight fell sharply
from 50.6 to 47.6 kg. On Nov. 23, 300 gm. thrice cooked vegetables were given
to appease the patient, who was discontented. This program continued up to
and including Dec. 1. As such vegetables are reckoned as having too little food
value to count, the treatment represents 2 weeks of practically continuous fasting
except for the alcohol mentioned. The continuance of glycosuria aroused sus-
picion. Accordingly the patient was removed from the ward to a private room,
and glycosuria abruptly ceased (Nov. 26). He was then returned to the ward,
and was sufficiently impressed by his sugar-freedom that he followed diet with
some degree of fidelity thereafter, though some of the traces of glycosuria are
doubtless to be attributed to slight violations. A low diet was begun, and it was
found that the tolerance was actually very low, the smallest quantity of carbo-
hydrate bringing on glycosuria, while even on protein-fat diet traces of sugar were
frequent, apart from any steaUng of food. The patient was discontented and
unreliable, and the irregular shifts of diet resulted largely from attempts to please
him. The general outcome of the treatment was to reduce his weight from the
original 50.6 kg. to 44.8 kg., with the result that glycosuria was absent on a car-
bohydrate-free diet of 53 gm. protein and over 2200 calories, but a well marked
ferric chloride reaction persisted. Thorough treatment was not carried out
because the patient had never been seriously iU and would not have endured
rigorous measures. Accordingly he was allowed to go on Mar. 2, with his con-
dition improved but by no means satisfactory, on a prescribed diet of about 50
gm. protein and 1500 to 1750 calories.

Subsequent History. — On Apr. 1, patient returned to the hospital reporting that
he had followed diet, had remained permanently sugar-free, had gained 6 pounds,
and was enjoying greatly improved health. His appearance conformed to the

240 CHAPTER m

statement, but a sample of urine showed a trace of sugar. Information from other
quarters indicated that he had not adhered strictly to his diet. On Apr. 9, he
again reported and his urine was found sugar-free. On May 20, he reported
showing a slight glycosuria, and information was given by his family that he had
departed somewhat from his diet. Since then nothing has been heard of him.

Remarks. — ^The case illustrates diabetes of long standing, apparently doing the-
individual little harm but bringing progressive injury in the course of years,
and undoubtedly destined not only to impair comfort and usefulness, but also
to shorten life. As frequently found in such cases, a normal state of the urine is
very diflBicult to establish and maintain, and rigorous restriction of food and re-
duction of weight for a number of months are necessary for a satisfactory re-
sult. Such patients are often not convinced that these measures are necessary,
especially since they feel decidedly worse during the period of rigorous restric-
tion. FideUty brings ultimate reward in comfort and longevity. On the other
hand, the penalty of carelessness is often slow in appearing, and accordingly the
lesson is often learned too late.

CASE NO. 15.

Male, married, age 42 yrs. Scotch; bookkeeper. Admitted Nov. 16, 1914.

Family History. — ^Entirely negative as far as can be learned from wife.

Past History. — Healthy life.

Present Illness. — Patient is known to have had diabetes for about 2 y^ars past,
with practically no symptoms except some loss of weight and strength. He has
continued at his work until the present week. He was not supposed to be seri-
ously unwell until last evening, when a doctor was sent for hurriedly and found
him in coma to such a degree that he could not be roused enough to recognize
persons. The physician cleared out considerable feces by the use of cathartics
and enemas and gave a few small doses of sodium bicarbonate by mouth. This
morning the patient was stiU in coma, but was apparently a little more easily
roused.

Physical Examination. — Fairly good muscular development along with moderate
emaciation. Routine physical examination negative. Kjiee jerks absent. The
usual picture of coma, except that h3Tjerpnea is not striking. Respiration is
fuU, but quiet. When forcibly roused the patient regains consciousness suffi-
ciently to utter words in drunken meaningless fashion, but not to recognize his -
wife or doctor. With some difficulty he can be induced to swallow medicine and
to pass urine.

Treatment. — ^This was the first case of actual coma received, and the orthodox
treatment was attempted, with an intravenous infusion of 1 liter of 4 per cent
sodium bicarbonate solution prepared without heat and sterilized by filtration
through porcelain. The injection was apparently well borne; pulse, respiration,
and consciousness showed no appreciable, change during the period of injection,
which lasted about an hour. IS cc. whisky were given hourly. The patient

CASE RECORDS 241

was received at 5 :30 p.m. The infusion was finished at 7 p. m., and death occurred
suddenly and without warning at 7:50 p.m.

The following laboratory data may be noted. Heavy glycosuria and ketonuria
both before and after bicarbonate infusion, not determined quantitatively because
of loss of considerable urine. Blood sugar 0.316 per cent. Sodium chloride in
serum 6.11 gm. per liter. Sodium chloride in urine 0.2 gm. per hter before in-
fusion. The urine passed after bicarbonate infusion was pale and abundant as
before, but contained no chlorides.

Remarks. — Though few patients ever come out of actual coma, this man was
one who appeared to have a fighting chance. At that time it was hoped that
the alkali in the customary dosage would reinforce whatever benefit he might
derive from fasting. Without the intravenous alkali he might have had a chance.
Later experience makes it seem probable that when a patient in this condition
receives an injection of alkali in this manner and quantity, no immediate harm
and sometimes an apparent benefit is perceptible, but sudden death is likely to
occur within a few hours.

CASE NO. 16.

Female, married, age 47 yrs. American; housewife. Admitted Nov. 17,
1914.

Family History. — Father died of cancer at 61. Mother had diabetes; died of
sepsis from varicose veins in legs at 74. Brother aged 61 has mild diabetes.
Patient's husband died 20 years ago, aged 34, of some condition resulting from
alcoholic excess. Three chUdren; the two older living and weU; the youngest
was mentally deficient and died last July at the age of 20, after having been
treated from childhood for syphilis.

Past History.— Healthy childhood. Measles and mumps when very young.
Chlorosis before marriage. Married at 20; two children within a year of each
other; no miscarriages. Third child, born 4 years after second, showed syphilis,
and patient after its birth had sore on tongue and hair fell out. There was also
a genital chancre. Symptoms cleared up after 1 month of treatment with blue
ointment. No further symptoms or treatment. Regular habits. No excess in
alcohol, tea, coffee, or sweets. Never nervous until recent years. Ordinary
weight 180 pounds.

Present Illness. — 5 years ago patient began to feel weak and lost 20 pounds in
weight. Physician found glycosuria of 4§ per cent. She has dieted more or less
since then, but has been sugar-free only occasionally, never more than a few
months. Lowest weight 143 pounds last August. Menstruation stopped 6
months ago. Especially for the past 3 weeks she has felt weak and miserable and
been troubled with thirst, headache, pains in knees, cold feet, pruritus vulvae,
failing vision, and loosening and falling out of teeth.

Physical Examination. — Height 158 cm. A rather obese woman, looking
strong but nervous. Several teeth missing; others loose. Throat normal. No

242 CHAPTER m

palpable lymph node enlargement. Murmur of mitral regurgitation. Area of
cardiac dulness slightly enlarged. Arteries hardened. Blood pressure 225
systolic, 110 diastolic. Albumin and casts in urine. Knee and Achilles jerks
slight. . A few small copper colored scars on legs. Uterus sUghtly retroverted.
Right Fallopian tube slightly tender. Blood shows strong Wassermann reac-
tion. In addition to diabetes, there was a diagnosis of chronic mitral insuffi-
ciency, chronic interstitial nephritis, latent syphilis, arteriosclerosis, and cystitis.
Twice during hospital sojourn the patient complained of dizziness and fainted,
and was treated for short periods with digipuratum. Syphilis was not treated
at this time, and the effect of dietetic treatment of the diabetes was tested alone.

Treatment. — ^As shown in graphic chart, the patient fasted Nov. 18 to 20 inclu-
sive, receiving respectively 45 and 75 cc. whisky on the last 2 days. On Nov.
21 she received cauliflower, celery, and asparagus to the amount of 17.5 gm. car-
bohydrate. As the primary object was to reduce weight, 3 more days of practi-
cal fasting (Nov. 22 to 24) followed, the only food being 800 gm. thrice cooked
vegetables daily. On Nov. 25, one egg was added. This diet was rapidly in-
creased to about 1100 calories on Dec. 6 and 2300 calories on Dec. 19. AU at-
tempts to introduce even small quantities of carbohydrate led to glycosuria, and,
as shown in graphic chart, numerous periods of low diet or fasting were employed
to diminish the weight further. She was finally (Jan. 27 to 29) placed on a car-
bohydrate-free diet of 66 gm. protein and 1400 calories. This, for her weight of
54.5 kg. at that time, was about 1.2 gm. protein and 26 calories per kg. The pa-
tient insisted that this diet with addition of 500 gm. thrice boiled vegetables satis-
fied her appetite perfectly, and as she was very eager to be home and had received
the necessary instruction, she was allowed to leave in this condition. All sub-
jective symptoms had disappeared and she felt fuUy strong and well.

^Subsequent History. — The progress continued to be favorable at home, and in
Feb. the diet was increased by 400 calories of bacon. Sugar remained constantly
absent and the ferric chloride diminished to a trace. It became entirely negative
about June 1. The plasma sugar on June 1 was 0.114 per cent. The weight
was 54.5 kg. By Oct. 5, the patient had gradually increased the quantity of food,
the weight had risen to 59.8 kg., and the plasma sugar to 0.196 per cent, with nega-
tive sugar and ferric chloride reactions in urine. Blood pressure 250 systolic, 160
diastolic. She was advised to avoid gaining weight. Excellent subjective
health and normal urine continued, and 1 year after discharge she reentered the
hospital by request for examination and advice.

Second Admission. — ^Jan. 31, 1916. The weight at this time was 63 kg.; namely,
8.6 kg. above that on dismissal and 2 kg. below that at former admission. The
urine showed negative sugar but a trace of ferric chloride reaction. Feb. 2 a fast-
day was given, and then a carbohydrate tolerance test, begiiming with 10 gm.
carbohydrate and increasing by 10 gm. daily vmtil by Feb. 23 to 25 the limit of
tolerance was reached with 220 gm. carbohydrate. After a fast-day on Feb. 27
to clear up the slight glycosuria, a diet was instituted of 90 gm. protein, 20 gm.

CASE RECORDS 243

carbohydrate, and 2000 calories (1.5 gm. protein and 34 calories per kg., reduced
by weekly fast-days to about 1.3 gm. protein and 30 calories average). On this
diet the patient was dismissed, weighing 59.5 kg.

Acidosis. — The patient was admitted originally with chronic glycosuria and
negative ferric chloride reaction. The result of fasting, notwithstanding 75 cc.
whisky on Nov. 20 and 17.5 gm. carbohydrate on Nov. 21, was the development
of a ferric chloride reaction. This persisted during most of the first stay in hos-
pital. It could doubtless have been cleared up by repeated periods of carbohy-
drate (without other food) to the limit of tolerance. But the tolerance at that time
was low, and for a patient with such inherently mild diabetes at a fairly advanced
age, it was considered sufficient to pursue a treatment of progressive undernu-
trition, knowing that the trivial acidosis would disappear as soon as the tolerance
was built up. This expectation was fulfilled in the period after leaving hospital.
With rise of weight, traces of ketonuria had returned at the time of second admis-
sion; these were readily cleared up by the carbohydrate tolerance test, and by
increasing carbohydrate in the diet. Since then ketonuria has remained per-
manently absent. As shown in the second graphic chart, the plasma bicarbon-
ate was slightly below the lower normal limit; but the tendency was upward, and
no alkali was employed.

Blood Sugar. — ^This was easily kept at normal level by regulation of body weight.
On this point the patient might be brought into line with the type formerly called
"fat sensitive." It wiU be observed in the second graphic chart that hyper-
glycemia was present on Feb. 2 after a diet of 2350 calories made up chiefly of
fat with very little carbohydrate. This elevated blood sugar is seen to have fallen
to normal subsequently when the carbohydrate was decidedly increased and the
total calories diminished. Though nephritis and arteriosclerosis were present
with hypertension, there was no tendency to a stubbornly high blood sugar.

Subsequent History. — The patient has reported at intervals to date, feeling en-
tirely healthy and leading a fully normal life with faithful attention to diet.
Weight June 19, 1917, 63.6 kg. This increase of weight has been borne with&ut
any glycosuria. The high blood pressure remains, also the albumin and casts in
urine. Lately she has complied with advice given several times before and has
taken a few salvarsan injections, without alteration of clinical findings. The
cardiorenal symptoms are perceptibly increasing, and death from this cause is to
be expected.

Remarks. — Two possible etiologic factors are here present, one heredity, the
other syphilis. Notwithstanding these, and even in absence of syphilitic treat-
ment, the entire tendency under suitable dietetic treatment through nearly 3
years of observation has been upward and not downward. This success has been
attained by regulation of the total caloric ration and body weight. It is practi-
cally certain that a progressive downward tendency could have been observed if
the weight had been built up with high calory, carbohydrate-poor diet. Such a
tendency is distinctly indicated by the findings at several times when weight was

244 CHAPTER ni

gained. Another interesting feature is that in Apr., 3 months after the first
dismissal, the patient had an acute otitis media and underwent paracentesis under
ether, but showed no sugar throughout this illness. From present indications the
prognosis in such a case is satisfactory from the standpoint of diabetes, and life
and comfort are apparently limited only by the other diseased conditions present.

CASE NO. 17.

Female, married, age 69 yrs. Russian Jew; housewife. Admitted Nov. 17)
1914.

Family History. — Indefinite on account of ignorance. Most of family seemingly
lived to considerable age, and patient knows of no family diseases. Patient has
been married 43 years. Seven children; four died in infancy, cause unknown; one
is in a pubhc institution with diagnosis of dementia praecox; the other two are
middle-aged and well.

Past History. — Measles in childhood. Came to New York from Russia 26
years ago. Hygienic surroundings bad. No diseases of consequence, except em-
pyema with pneumonia 20 years ago. This was drained, and two subsequent
operations were necessary before the sinus was closed a year later. She has had
no s)rmptoms pointing to tuberculosis. She has long complained of indigestion,
gas, and constipation. 6 years ago she underwent an operation for uterine pro-
lapse; there was a laparotomy and removal of some sort of tumor, concerning
which she knows nothing except that it was not cancer.

Present Illness. — ^Time,of onset unknown, but during the past 7 years her weight
has steadily diminished from 180 down to 108 pounds. Polyphagia never marked,
and polydipsia noticed only in the past few days. 6 weeks ago pain began in
the right foot with some discoloration around the great toe and heel. Local
measures did not benefit it. A physician suspected gangrene immediately upon
seeing it and found heavy glycosuria present. This was the first diagnosis of
diabetes. She is now unable to walk because of pain in this foot, which is also
painful when she remains in bed.

Physical Examination. — Patient fairly nourished, lying in bed with quiet respira-
tion, but with decided sweet odor of breath. Dirt and pedicuH noticeable. Nu-
merous teeth missing or carious. No gland enlargements except in groins. A
few bronchitic rales. Heart sKghtly enlarged. Blood pressure 215 systolic, 150
diastoUc. Depressed scars on left thigh, pigmented scars on right shin. Swell-
ing, reddish blue discoloration and tenderness of great toe and over and under
first and second tarsometatarsal joints of right foot. The heel of this foot is
painful, the skin is Hfted up and evidently has fluid under it.

Treatment. — Patient received supper on the day of admission, consisting of 25
gm. AkoU biscuit, 10 gm. butter, and a cup of coffee. The next day she fasted
with 35 cc. whisky, and became sugar-free in 24 hours. The ensuing days were
also fast-days, with whisky up to 90 cc. On Nov. 23, one egg and 300 gm. thrice

CASE RECORDS

245

boiled vegetables (cauliflower and asparagus) were added. The diet was then
rapidly increased, particularly in its fat component,, as shown in Table IX.

It is seen that the great increase of fat intake on Nov. 29 was accompanied by
sharp increase of both glycosuria and ferric chloride reactions. The simul-
taneous increase of protein in the diet did not serve to prevent this increase of
acidosis. Also it is difficult to attribute the glycosuria of 11 gm. to the increase of
only 5 gm. protein on Nov. 29, as compared with the preceding day. Further-
more, though this glycosuria was only 11 gm., because the high diet was composed
chiefly of fat, the injurious after-effect is likewise characteristic of fat. For the
entire first week in Dec. the diet was only once as high as 500 calories; Dec. 5, 6,
and 7 were fast-days with alcohol, yet the aglycosuric condition was difficult to
restore. Beginning Dec. 8 the attempt was made to build up a diet, beginning
with eggs, butter, and 'thrice cooked vegetables. Whisky was never entirely
discontinued, and in Jan. the intake represented about 65 gm. alcohol daily.
The protein was generally 40 to 60 gm.; i.e., a httle above or below 1 gm. per kg.

TABLE rx.

Date.

Diet.

Weight.

Urine.

Protein.

Fat.

Alcohol.

Calories.

Volume.

Sugar.

FeCb
reaction.

1914

em.

em.

am.

ke.

cc.

em.

Nov. 27

47

135

43

1746

50.6

1540

+

-f-l-H-

" 28

57

179

15

2005

51.6

2005

+

++

" 29

62

509

15

5096

50.5

1115

11.15

-1-4- H-

" 30

37

259

10

2629

51.3

1190

+

+++

Dec. 1

37

259

15

2664

51.0

860

+

++

of weight. The calories were kept at approximately 1000 to 1200, or about 20
to 24 calories per kg. for SO kg. body weight. The traces of glycosuria indicated
in the graphic chart were very slight, and were mostly connected with the use of
thrice cooked vegetables. The tolerance for carbohydrate was so low that
300 to 500 gm. of vegetables of Joslin's 5 per cent class, boiled through three waters
in the usual way, brought on these traces of glycosuria. In Jan. these vegetables
were omitted. The patient being an old woman with small appetite, it was pos-
sible to place her on a ration made up of coffee, soup, whisky, eggs, meat, fish,
butter, and olive oil. She remained practically sugar-free on this regimen, since
the traces of glycosuria noted thereafter were mostly very faint reactions in the
urine of single periods during the day, undiscoverable if mixed with the 24 hour
urine. The undernutrition is indicated by the continuous fall in weight during 2|
months, from 53.5 kg. on admission to 45 kg. on discharge. She was discharged
on Feb. 1, very happy with her condition. The incipient gangrene had healed
early, and she had been restored to comfort and activity. She felt able to con-

246 CHAPTER in

tinue her diet amid the difficulties of her home conditions. Slight albuminuria
and casts present on admission still continued at discharge, and the systolic
blood pressure was 205 mm.

Subsequent History. — The patient was unable to continue her diet successfully
at home. As she evidently required continuous care, she was advised to enter
a semipublic institution, where she has since lived and is kept on a moderately
restricted diet, with 1 to 3 per cent sugar constantly in the urine and continual
pain in the right foot, which does not completely disable her and has not been
accompanied by any return of actual gangrene.

Acidosis. — ^As respects acidosis, it will be noted that she entered with a nega-
tive ferric chloride reaction, evidently because of the carbohydrate in her former
diet. The ferric chloride reaction appeared on the 4th day of fasting, about as
might be expected in a normal person, and it is again nonceable that 300 calories
of alcohol did not prevent the appearance of this reaction. The reaction was
never a heavy one, and in a feeble woman of this age it was not considered ad-
visable imder the circumstances to impose the rigorous measures which wovdd
have been necessary to make the urine quickly normal. Theoretically, this con-
tinued slight acidosis and the diet keeping her barely on the verge of glycosuria
all the time were wrong, and under ideal conditions actually better results could
have been achieved by more rigid measures, cutting her diet and weight still
lower and bringing about a normal state of the urine and at least some slight
carbohydrate tolerance. Practically, there was a strong likelihood that she
would not be able to foUow the necessary diet outside the hospital, and it seemed
therefore unwise to attempt an ideal result. Under the plan pursued, her condi-
tion at discharge was a good one for her years, and by persisting in the same
program she would almost certainly have gained gradually some carbohydrate
tolerance and lost her trace of acidosis; but her mental and social state interfered
with this result.

Remarks. — This patient was admitted as presenting early diabetic gangrene
with seniUty and arteriosclerosis, the idea being to test the effect of therapy in
such a case. Simple protection and occasiohal hot air baths were the only local
measures employed, but healing proceeded uninterruptedly and apparently as
rapidly as possible at this age. It was striking that pain in the foot could at
first be produced at wiU by food. Excessive diet which brought return of glyco-
suria was found to bring complaint of pain the same day, although the patient
was kept ignorant of the laboratory tests. On discharge the foot appeared
entirely normal, except for coldness to touch and some loss of tissue in the for-
merly discolored areas. Pain, tenderness, and disability had disappeared. The
loss of weight under treatment, amounting to about one-seventh of her entrance
weight, did not serve to weaken her. On the contrary, she went out with improved
strength.

The case well illustrates a familiar therapeutic situation. In numerous cases
of diabetes in advanced senility, in one sense the diabetes is mild, the glycosuria

CASE RECORDS 247

is not excessive, the acidosis does not threaten coma, and the patient seems to
go along for years "with little injury. Some form or degree of harm ordinarily
results sooner or later, frequently, as in this case, gangrene. On treatment, the
apparently mild diabetes proves by no means easy to control. The tolerance
from the standpoint of complete sugar-freedom is surprisingly low, and months
of privation and reduction of weight and sometimes also of strength are neces-
dary to atone for the harm caused by years of lack of care. Only three courses
are open. One is rigorous and conscientious treatment, just as in a younger
patient. This is diflScult and tedious for both physician and patient; but when
circumstances permit it to be carefully carried out, the ultimate results are more
favorable than in younger persons, and the improvement of health and appar-
ently of longevity prove that the previous glycosuria was not harmless but was
largely responsible for symptoms attributed to senility or other causes. The
other extreme is complete disregard of diet. This course may be expected to
bring death from gangrene or other accident, sometimes even coma, in a large
proportion of patients. Here again due weight may not be given to diabetes as
the predisposing cause back of the infection or other terminal condition. The
middle course is one frequently adopted; namely, a moderate regulation of diet
with the aim of preserving strength and comfort and not paying too much attention
to laboratory findings. In the case of this patient, the alleged comfort of such a
course consists actually in continuous pain in the right foot and the danger of
gangrene at any time. It is also scarcely reasonable to suppose that the foot is
the only part of the body injured by the diabetes.

CASE NO. 18.

Male, unmarried, age 16 yrs. American; errand boy. Admitted Nov. 18,
1914.

Family History. — Grandparents' history not certain. Father died at, 42 of
cirrhosis of liver. Mother and two sisters of patient alive and well.

Past History. — Healthy life. Chicken-pox at 6. Tonsillitis in 1912. No
other iUnesses. Habits regular. No alcohol, very little tobacco. No exces-
sive sweets or carbohydrate. Never nervous. Ordinary weight 133 pounds.

Present Illness. — Only 3 weeks ago, during the last week of Oct., first symptoms
were noticed in the form of thirst, polyuria, polyphagia, weariness, and sleepiness.
During present month he has been unable to read by artificial light because of
blurring. Nov. 1, he stopped work and consulted a physician, who found 5 per
cent glycosuria. Patient claims to have followed restricted diet since then, in-
cluding gluten bread. He has never become sugar-free.

Physical Examination. — ^Normal in appearance though rather thin and nervous.
Teeth in good condition. Tonsils slightly enlarged. A few small palpable
glands in neck. Knee and AchiUes jerks exaggerated. Blood pressure 135
systolic, 60 diastolic. Examination otherwise negative.

248 CHAPTER m

Treatment. — The diet on Nov. 19 consisted of 105 gm. protein, 17 gm. carbo-
hydrate, and nearly 2000 calories. The glycosuria diminished to traces, and sugar-
freedom could doubtless have been readily attained without fasting. Neverthe-
less, for the sake of more rapid and radical improvement, 4 days of fasting were
imposed (Nov. 20 to 23). To make the fast easier, thrice cooked vegetables in
quantities increasing up to 1500 gm. daily were permitted. The trace of ferric
. chloride reaction which developed cleared up spontaneously.

On Nov. 24 two eggs and 20 gm. butter were added, increased on the next
day to four eggs and 40 gm. butter. Meat and bacon were subsequently added.
The negative ferric chloride reactions, Dec. 1 to 4, on diets of 2200 to 2300 calories
without carbohydrate and composed chiefly of fat, stand in strong contrast
with what other patients often show when sugar-free on the same sort
of diet. Thereafter the patient proved able to tolerate as much as 2900
calories with 60 to 80 gm. carbohydrate and 107 to 130 gm. protein. He was
dismissed on approximately this diet but with calories diminished to about 2500.
. General instructions were given, but the food was not required to be weighed.
The liberal diet (over 2 gm. protein and 50 calories per kg.) was permitted with
the idea of satisfying the patient and allowing him to work hard, and in the hope
that it might be tolerated in view of the early and mild stage of the diabetes.
The average was reduced slightly by the fast-day ordered ev^ry 2 weeks. Also
instead of weighing food, the patient was instructed to keep careful account of
his own weight and never let it go above 120 pounds {i.e. 13 pounds below his full
normal weight). Any gain over this was to be checked by fasting and reduced
diet.

Subsequent History. — Reports indicated that the patient adhered to his diet
until cherries became ripe in summer, when he started glycosuria by eating cher-
ries. As he then broke diet in other respects, he was instructed to return to the
bospital on July IS.

Second Admission. — In addition to glycosuria, decided ketonuria was present
this time, notwithstanding 125 gm. carbohydrate in the diet on July 16. 3 days
of fasting with nothing but cofiee and soup were imposed Quly 18 to 20), followed
by a carbohydrate tolerance test, starting with 20 gm. carbohydrate in the form
of green vegetables. The quantity was increased by 20 gm. carbohydrate daily,
until on Aug. 4, 350 gm. carbohydrate were taken without glycosuria. Without
attempting to push the carbohydrate higher, a fast-day was given on Aug. 5, with
only coffee and soup. A diet was then instituted of 100 gm. protein, 100 gm. car-
bohydrate, and 2600 calories. Later the carbohydrate was raised as high as 200
gm. Traces of glycosuria occurred on this diet. It is noteworthy that even with-
out glycosuria and with this high carbohydrate intake, some distinct ferric
chloride reactions were present. On Aug. 21, the carbohydrate was diminished
to 5 gm., the protein remaining about 100 gm., and the total diet about 2500
calories. On Aug. 28, 100 gm. carbohydrate were resumed, and the protein and
total diet diminished to 84 gm. and 2400 calories respectively. The patient was

CASE RECORDS 249

discharged on this diet. His weight was 56 kg. at this admission, {i.e. a return
to his full normal weight which had been forbidden) and 51.8 kg. at discharge
(still about 1 kg. higher than at his first admission) .

Subsequent History. — Nothing further was heard from the patient until a letter
from his sister.reported his death on Nov. 11, 1915. Inquiries revealed that the
mother had no control over the boy, who refused to foUow diet or allow his urine
to be tested. The physician who referred the boy to this hospital was out of
town. After the usual polyuria, polydipsia, and loss of weight and strength, the
patient late in Oct. began complaining of indigestion, and a few days before death
showed a high degree of nervousness and excitement. A local physician treated
these symptoms of acidosis with tablets for the indigestion, sedatives for the
nervousness, and tonics for the weakness. Heavy breathing was noted at the end,
but actual coma was only a few hours in duration.

Remarks. — ^The condition was at a very early and favorable stage when treat-
ment was begun. The well marked ferric chloride reactions without glycosuria
on the high carbohydrate diets of Aug. 16 to 20 possibly indicate the intrinsic
severity of the case. Undoubtedly the violations of diet and the gain in weight
between the two admissions constituted a serious setback. Nevertheless, the
carbohydrate test up to Aug. 4 showed that the tolerance was still high, and the
blood sugar later in Aug. was found to be easily brought to normal. The later
course was the t3rpical uninterrupted downward progress of severe untreated dia-
betes, owing entirely to the fault of the patient and of the local practitioner who
then treated him. No dietetic treatment could accomplish anything in a patient
so irresponsible as this.

Concerning the diets prescribed in the hospital the following may be re-
marked. The change to practically carbohydrate-free diet on Aug. 21 is the
typical old-fashioned method. It is observed that in spite of the high caloric
intake (nearly SO calories per kg.) the blood sugar promptly fell to normal and
the results might be called favorable. The fact is that the ferric chloride reaction
persisted, and continuance of such a high intake would inevitably have brought
disaster later, no matter how favorable the laboratory findings for the time being.
The diets allowed this patient were unduly high, for the following reasons. First,
it had not yet been established whether the patient at such an early stage might
recover sufficient tolerance to carry the fuU load of diet and weight. Second, this
patient was given exercise involving considerable labor (see Chapter V), and it
was anticipated that he would perform considerable muscular work at home.
Third, it was evident from his general character that he would not endure any
real privations, and he was therefore placed on a diet which left no excuse for
violations, being fuUy satisfactory in protein, carbohydrate, and total quantity,
and calling only for abstinence from sugar and reasonable limitation of starch.
As stated, later experience has made it evident that such treatment is bad, and
always results in the downward progress which was formerly regarded as spon-
taneous and inevitable. The attempt to try this method in this case failed on
account of the patient's disobedience.

250 CHAPTER ni

CASE NO. 19.

Female, married, age 39 yrs. Russian Jew; housewife. Admitted Nov. 18,
1914.

Family History.— Pa.ients lived to old age. Patient had four brothers and nine
sisters; all are living or died of typhus or accidental causes in Russia. No dia-»
betes, cancer, tuberculosis, syphilis, or nervous diseases known in family.

Past History.— Born in Russia; came to United States 26 years ago. Hy-
gienic surroundings poor. Measles and whooping-cough in childhood. Typhus,
at 12. 16 years ago a so called abscess in throat, said to have been cured by
lancing. 7 years ago patient had a convulsion after a confinement; had to be in
hospital 3 weeks and was sick for 3 months. Some shortness of breath on exer-
tion for 2 years past. She was married 18 years ago. Husband Uving and well.
Four children living and well; one born dead, full term; one miscarriage. Habits
regular, no excesses. Frugal diet, poor in sweets but also in vegetables.

Present Illness. — ^Began with pruritus vulvae li years ago. A doctor pre-
scribed a salve which was ineffective. 1 year ago polydipsia commenced. She
drank 60 glasses of water a day. Polyphagia began 6 months ago. She has lost
38 pounds during the past year, falling from her normal weight of 146 pounds
to 108 pounds. Sleeplessness, weakness, pains in back also complained of. She
consulted two different physicians who, notwithstanding these typical symptoms,
told her she was "run-down" and prescribed tonics without examining urine.
4 weeks ago she came to New York for further medical advice. Diagnosis of
diabetes was made and she was in a hospital for 2 weeks on a diet limited abso-
lutely to meat, eggs, fish, cream, cheese, and string beans. Her condition failed
to improve, and on her physician's advice she made apphcation at this Institute.
Her chief complaints are extreme weakness and persistent headaches.

Physical Examination. — A well developed woman without evident discomfort
or dyspnea, appearing only sUghtly undernourished, but with flabbiness of skin
indicating considerable loss of weight. Nephritic countenance, with slight edema
about eyes and general pallor. Ocular examination negative. Teeth show
neglect; many missing; those remaining show caries and pyorrhea. Throat ap-
pears normal. Heart normal. Slight empyema. Reflexes normal. Examina-
tion otherwise negative. Blood pressure 90 systolic, 70 diastolic. Wassermann
negative.

Treatment. — (No graphic chart.) On her first day in hospital (Nov. 18) the
patient received a carbohydrate-free diet of 12 gm. protein and 411 calories, and
excreted 8.3 gm. sugar. Notwithstanding the great weakness complained of and
the presence of nausea and colic, fasting was begun the next day and continued
for 5 days. Alcohol was permitted because of weakness, but not more than 80
cc. whisky per day could be taken because of nausea. The ferric chloride reaction
was negative on admission, positive on the first fast-day and diminished so that
it was fully negative like the sugar reaction on the 3rd day of fasting. 180 gm.

CASE RECORDS 251

thrice cooked vegetables were given on the 4th and 5th days. A very low diet
was then begun, consisting of two eggs and 500 gm. thrice boiled vegetables.
The weight, which was 47.2 kg. on admission, diminished to 44.6 kg. on Nov. 24.
The patient complained of great hunger. The diet was rapidly increased until on
Dec. 5 it consisted of 60 gm. protein, 2 gm. carbohydrate, and 3600 calories.
This was tolerated without glycosuria or ketonuria, but the carbohydrate toler-
ance was very low. On Dec. 7 the addition of 200 gm. green vegetables con-
taining 9.8 gm. carbohydrate resulted in shght glycosuria. The weight by this
time was up to 48.8 kg. and the patient was much improved subjectively. The
glycosuria was checked by a fast-day with 45 cc. whisky, then carbohydrate-free
diet resumed, at first very low (25 gm. protein and 250 calories), but again rapidly
increasing until on Dec. 19 it contained 138 gm. protein and 3330 calories. The
attempt to include 7 to 12 gm. carbohydrate in the form of green vegetables
again resulted in slight glycosuria. Without a fast-day, the carbohydrate was
stopped and the total diet diminished to 600 calories, followed by an increase as
before. On Dec. 28 the weight was 47.4 kg., and a diet of 100 gm. protein and
22 gm. carbohydrate were tolerated without glycosuria. The same was true of
the diet of 91 gm." protein and 27 carbohydrate on Dec. 29. The assimilation of
carbohydrate here is explainable by the lower weight and the lower total diet;
namely, 2200 calories on each of these days. Likewise 103 gm. protein, 24 gm.
carbohydrate, and 2400 calories were tolerated on Dec. 30. The patient was
discharged on Jan. 3, 1915, on a carbohydrate-free diet of 110 gm. protein and
2500 calories, with 600 to 800 gm. thrice cooked vegetables daily. She felt well
and fit for work and was continuously free from both glycosuria and ketonuria.
Her weight at discharge was 47.6 kg., or practically identical with the weight at
admission.

Subsequent History. — The patient followed her diet faithfully, and on Apr. 20
the addition of 10 gm. carbohydrate was permitted. Her weight tended to in-
crease, and was 50.4 kg. on Aug. 2, 1915, and 55.8 kg. on Jan. 11, 1916. She was
then instructed to take a fast-day once every 2 weeks. One feature of her his-
tory is that 7 weeks after discharge (Feb., 1915) and again in Nov., 1915, she had
severe colds or grippe with fever, which confined her to bed 1 or 2 weeks, while
no more than traces of glycosuria appeared. Her progress continued steadily
favorable, and in Jan., 1916 she was referred to another clinic for further guidance
and observation. She was seen again in Apr., 1918, still following diet and doing
her housework without complaint.

Remarks. — The case gives the usual illustration that the way for a weak and
undernourished diabetic to gain strength and well-being is by therapeutic under-
nutrition. Abrupt initial fasting is sometimes dangerous in patients showing the
condition here described at the outset, but was well borne in this instance. With
sugar-freedom and loss of weight, the patient felt distinctly better; and in view
of her age and the relative mildness of the case it was considered safe to augment
her diet rather rapidly. As is frequent in such cases, with an adequate ration of

252 CHAPTER ni

protein and calories, the carbohydrate tolerance was practically nil. With the
weakened condition and the apparent absence of tolerance, this might have been
classed in standard text-books as a severe case. The relative mildness was
shown by the steady improvement when the urine was merely kept sugar-free.
It is also of interest that occasionally patients of this sort, handicapped by ignor-
ance and poverty combined, prove able to follow diet with fidelity, test their urine
conscientiously, and achieve satisfactory results.

CASE NO. 20.

Female, married, age 38 yrs. American; housewife. Admitted Nov. 19,
1914.

Family History. — One brother died of tuberculosis at 29 years of age. Family
otherwise healthy.

Past History. — Scarlet fever, measles, chicken-pox, whooping-cough, and
diphtheria all before 7th year. Also at age of 2 patient had a fall injuring left
knee so that she was unable to walk until 13, and the leg is stiU stiff. Has had
headaches all her life. Lately they are limited to the menstrual period, and are
localized in migraine fashion on the left side of the face. Numerous sore throats
during the past year. Habits regular. No excesses, no special fondness for
sweets or starches. Married 13 years ago. One child born 12 years ago died of
heart trouble a few hours after birth. A second living and well. Venereal dis-
eases and symptoms denied.

Present Illness. — Glycosuria was discovered 1 year ago when patient went to a
hospital for another cause. Since then there have been no symptoms except the
gradual loss of SO or 60 pounds of weight. She has noticed a darkening of the skin
about her eyes during this time. This began in the form of small dots which have
increased and fused until they form a very noticeable broad brown ring around
her eyes. She has been on a moderately restricted diet with continuous glycosuria,
and has been taking sodium bicarbonate and citrate for the past few weeks.
Nervousness has developed and she tires easily. She was referred to the Insti-
tute by her physician on suspicion of bronzed diabetes.

Physical Examination. — Height ISO cm. A nervous, frightened looking woman,
well nourished, with sweetish odor of breath. Shghtly elevated bronzed circle
1| to 2 cm. wide about both eyes is most striking characteristic of face. Teeth
neglected, three missing, one carious; no pyorrhea. Throat normal. Heart
shows signs of well compensated mitral regurgitation. Blood pressure 140-
110. No enlargement of lymph nodes except in axilla. Knee jerks present
on right, absent on left (injured side). Examination otherwise negative. No
pigmentation except that about eyes.

Treatment. — Patient was first kept on an observation diet without fasting.
No special pecuharities were noticed, and she was able to tolerate 75 to 80 gm.
protein, 30 to 40 gm. carbohydrate, and 1500 to 1800 calories with no glycosuria

CASE EECOEDS 253

or only traces. Ketonuria was stubbornly persistent but never dangerous in de-
gree. Slight albuminuria present on admission cleared up completely and did not
return. The observation diet as a whole represented undernutrition, inasmuch
as the weight fell from 53 kg. at entrance to 48.5 kg. on Dec. 18. The condition
about the eyes proved to be xanthelasma, and nothing was found to indicate a
true bronzed diabetes. Accordingly a more radical treatment was instituted in
the latter part of Dec, especially with a view to reducing weight. From Dec. 20
to Jan. 6 the diet contained nothing but whisky and green vegetables. Traces of
glycosuria appeared when the carbohydrate intake was approximately 60 gm.
By this means the urine was at last made free from both sugar and ferric chloride
reactions (Jan. 5 and 6). Carbohydrate was then excluded by thrice boiling the
vegetables, and two eggs were added. The diet was then built up, so that on
Jan. 13 to 14 it consisted of about 80 to 90 gm. protein, 30 gm. carbohydrate, 60
gm. alcohol, and 2200 to 2300 calories. The weight had thus been reduced to
46.6 kg.; i.e., a loss of 6.4 kg. since admission. Though the ferric chloride reac-
tion had reappeared, it was deemed safe to let the patient go home on this theo-
retically excessive diet, in order that she might carry on her housework comfort-
ably and continue to improve in strength and nervous control, the expectation
being that in such a case and under such conditions the gradual gain in tolerance
resulting from continued sugar-freedom would take care of the persisting ab-
normalities, notably the ketonuria.

Subsequent History. — The patient adhered faithfully to her diet at home, car-
ried on her housework, nursed her daughter through pneumonia, gradually lost
her nervousness, and remained continuously free from glycosuria but with a
slight ferric chloride reaction constantly present, even with addition of 10 gm.
carbohydrate to the diet on Apr. 20. On June 2 she was readmitted to the hos-
pital because of complaint that she was not feeling so well and that her nervousness
was returning.

Second Admission. — The weight at this admission was 43.8 kg.; i.e., 2.8 kg.
less than at discharge. The general condition was much better than at the former
admission. The pigmentation about the eyes appeared neither to have increased
nor diminished. The urine was entirely free from sugar, as the patient reported
it had been continuously, but the ferric chloride reaction had become heavy, and
the 24 hour urine contained 1.96 gm. ammonia nitrogen. The symptoms com-
plained of were presumably associated with this acidosis. It was therefore
deemed desirable to proceed radically to abolish acidosis. This could not be
done by simple addition of carbohydrate to the diet, for on June 3 the giving of
30 gm. carbohydrate with 84 gm. protein and 1700 calories caused well marked
glycosuria. On the other hand, the acidosis diminished by simple reduction of
diet, so that on June 5, on a carbohydrate-free diet of 66 gm. protein and 1300
calories, there was excretion of only 0.56 gm. ammonia nitrogen. Therefore on
June 6 and 7, fast-days were given, with an allowance of 300 cc. coffee, 300 cc.
clear soup, and 50 cc. whisky. On Jime 8, alcohol was discontinued and never

254 CHAPTER III

again used for this patient. Green vegetables representing 10 gm. carbohydrate
were added on this day, and the usual carbohydrate tolerance test was instituted,
with increase of 10 gm. carbohydrate in green vegetables daily. A trace of gly-
cosuria appeared on June 14 with 90 gm. carbohydrate, but this did not represent
the true limit of tolerance, because glycosuria ceased, and the true limit was
reached only with about 150 gm. carbohydrate on June 23. Further increase
up to 170 gm. on the following days caused only slight but continuous glyco-
suria. Under this program the ferric chloride reaction became negative and the
ammonia excretion held a low level. After a fast-day on June 28, a regular
diet was gradually built up with one fast-day every week. Even with 37 to 45
gm. carbohydrate in the diet the ferric chloride reaction reappeared, but dimin-
ished, and on July 13 became negative with 67 to 75 gm. carbohydrate in a diet
otherwise composed of 75 to 100 gm. protein and 1600 to 2100 calories. The
weight on July 24 was 41.8 kg.; i.e., a loss of 2 kg. during this period in hospital,
or a loss of 11.2 kg. since her first admission. She was discharged to continue
this diet at home.

Subsequent History. — The patient continued to follow treatment faithfully,
and improvement continued with constantly normal urine. She passed through
an attack of grippe in Nov., 1915, without return of glycosuria. She has led a
fully normal life except for attention to diet, does her work easily, has lost all ner-
vousness, and feels well in every respect. In addition to her reports, she came
for personal examination on July 18, 1916. Her weight was then 45.2 kg.; i.e.,
a gain of 3.4 kg. since discharge. Her general appearance was excellent, with pig-
mentation unchanged. The urine was normal, the CO2 capacity of the plasma
50.3 per cent, the plasma sugar 0.189 per cent. This hyperglycemia received no
special treatment, for since there had been such obvious improvement before, it
was considered probable that it would continue, with ultimate reduction of blood
sugar, without more radical measures in a case of this type.

Remarks. — ^Aside from points abready noted, the case again illustrates the
benefit resulting from general therapeutic undernutrition in a patient who had
already suffered considerable loss of weight and strength from diabetes. Both
the treatment and the improvement were gradual in character. Results could
have been achieved more quickly by following up the alcohol-carbohydrate period
of Dec, 1914, with undernutrition sufficient to keep the ferric chloride reac-
tion negative, at the same time buUding up carbohydrate tolerance more rapidly.
As usual in such cases, however, the simple continuance of freedom from gly-
cosuria brought steady improvement, so that at the second admission there was
a considerable carbohydrate tolerance and acidosis was easily abolished without
interruption of the steady gain in well-being. The patient now weighs enough
for fully satisfactory looks, comfort, and strength. There is a complete con-
trast in these respects with her former condition at a higher weight. An at-
tempt to return to the former weight would doubtless bring a return of the
previous troubles. There has probably been little or no absolute improvement

CASE RECOEDS 255

in the power of assimilation, neither is there any evidence of any progressive
•decline. The patient is merely living within her assimilative power. As far as
-can be judged from the experience of nearly 3 years, she can continue to do so
without difficulty, and the general trend seems to be upward rather than
•downward.

CASE NO. 21.

Female, married, age 46 yrs. Scotch,* housewife. Admitted Nov. 20, 1914.

Family History. — Father died in accident. Mother died of heart trouble at
42. Patient was the only chUd. Diabetes, tuberculosis, cancer, syphilis, or ner-
vous disorders in any relatives denied. Patient married twice. Has had only
one child, who is alive and well; no miscarriages.

Past History. — Measles, mumps, and whooping-cough in childhood. Came
from Scotland to United States at age of 17. Scarlet fever 15 years ago. Op-
eration for ventral hernia 1 year ago. Subject to occasional headaches ever since
she can remember. Also has shortness of breath on exertion. Occasional sore
throats. No use of alcohol. Drinks six or eight small cups of tea daily. Up to
15 years ago weight was 146 pounds; since then it increased, so that at the time
of her operation a year ago it was 266 pounds. During this year she has lost
36 pounds.

Present Illness. — ^About 6 months ago patient began to notice polyuria, poly-
•dipsia, polyphagia, and increasing nervousness, with rapid loss of weight. These
have been the only symptoms. No treatment by diet.

Physical Examination. — ^Height 155 cm. A large framed, plethoric, obese
woman with dry skin, a nervous expression, and bilateral arcus senilis. Teeth
neglected, some missing; those remaining show caries and pyorrhea. Tonsils a
trifle hypertrophied. Slightly large thyroid palpable. No lymph node enlarge-
ment. Heart slightly enlarged. Slight emphysema. Knee jerks active. Leg
veins markedly varicosed. Blood pressure 175 systolic, 120 diastolic. Trace of
albumin in urine, but no casts.

Treatment. — ^The most obvious requirement was to reduce weight. The most
noteworthy initial observation was that in 4 days of absolute fasting this very
•obese woman failed to develop any ferric chloride reaction and showed abso-
lutely no symptoms of acidosis. On the following 4 days she received only mod-
erate quantities of whisky (not above SO gm. alcohol) . It is evident that they did
not prevent the appearance of a slight ferric chloride reaction. This reaction was
(negative on Nov. 28, when only 10 gm. alcohol were given, as if the larger quan-
tities of alcohol had tended to produce rather than prevent it. On Nov. 29, a
•carbohydrate-free diet of 93 gm. protein and 2260 calories caused a trace of
glycosiuia. The subsequent diets represent very marked undernutrition. It is
obvious from the graphic record that the patient not only had practically no car-
bohydrate tolerance but also tended to show traces of glycosuria even on very
low carbohydrate-free diets. She was of the type spoken of in older text-books

256 CHAPTER in

as relatively independent of diet ("paradoxical tolerance"). That is, her glyco-
suria had never been excessive, and if tested she would doubtless have proved her
abihty to assimilate most of the carbohydrate of any diet. Yet complete sugar-
freedom was difficult to achieve even with the most radical restrictions. Blood
sugar analyses were not made. It is probable that a continuous marked hyper-
glycemia was responsible for the frequent traces of glycosuria, and that this
varied Uttle with diet. The principal result of treatment was to bring the body
weight down from 108 kg. to 90 kg. No special attempt was made to conserve
the body protein. Nitrogen balances would undoubtedly have turned out strongly
negative. Nevertheless, there was a gain in well-being, and at discharge there were
no symptoms except those referable to arteriosclerosis, the former migraine attacks,
and other conditions apparently independent of the diabetes. The diet pre-
scribed at dismissal was approximately 75 gm. protein, 60 gm. carbohydrate, and
1300 calories, representing, for a weight of 90 kg., only about 0.8 gm. protein and
IS calories per kg. The trace of glycosuria on Jan. 24 may be regarded as of
the accidental type sometimes resulting from a sudden increase of carbohydrate.
It appeared that the patient could carry this diet without glycosuria and with a
bare trace of ferric chloride reaction. She stated that her appetite was reasonably
well satisfied, and she felt better when eating and weighing less. The trace of
albumin present in the urine at admission remained unchanged, but casts could
very seldom be found. The treatment was not considered complete at dismissal,
but undernutrition was to be continued at home.

Subsequent History. — The patient continued free from glycosuria at home,
with a persisting trace of ferric chloride reaction. She was not required to weigh
her food, and her estimates were probably enlarged with increase of appetite, for
her weight at first held practically even, being 90.6 kg. in Aug., 1915. By Oct.
there was an increase of 2.6 kg. The sugar in the whole blood was then 0.128 per
cent, in the plasma 0.161 per cent. Sugar remained absent from the urine; the
ferric chloride reaction continued present. She was instructed to fast 1 day every
2 weeks."

On Nov. 29, the weight was found to be 101.4 kg., plasma sugar 0.143 per cent,
CO2 capacity of plasma 43.2 per cent. The blood pressure was 240 systolic, 140
diastolic, and there had been symptoms referable to hj^jertension. She was
instructed to fast IJ days every week.

On Jan. 11, 1916, the blood pressure was 220 systoUc, 120 diastolic. The weight
was 101.5 kg. with clothing, 99 kg. stripped. She was instructed to remain in bed
for a week on a diet of nothing but low percentage green vegetables. The urine
was entirely negative for both sugar and ferric chloride reactions.

On July 13, 1916, the blood sugar was 0.128 per cent, plasma sugar 0.156 per
cent, CO2 capacity 56.9 per cent. Sugar and ferric chloride reactions in urine
remained negative. Though recent dietary instructions theoretically estab-
lished an intake of only 1000 calories, the patient's estimates were evidently too
high and the weight continued to rise, being now 103.2 kg. stripped. The patient

CASE EECORDS 257

has remained so well that she has not been closely supervised. She still con-
tinues to lead a normal life, and suffers only from headaches and occasional attacks
referable to hypertension.

Remarks. — Complication of this case with obesity and arterial hypertension
called for no special alteration in the treatment of the diabetes. The entire
condition rendered a reduction of weight desirable. By this simple measure
the carbohydrate tolerance, which appeared so very low, was easily raised, and
the case stood revealed in its true light as one of intrinsically mild diabetes. It
must again be mentioned that the initial stage of treatment of such a case some-
times presents difficulties and dangers such that fasting may have to be em-
ployed cautiously and after special preparation; but in this instance the fasting
offered no difficulty and the obesity was no obstacle to the gradual disappearance
of the ferric chloride reaction. The case thus opposes the idea that the available
' fat supply is the sole determining factor in fasting acidosis. Under a mild thera-
peutic regime hj^perglycemia has been persistent. It need not be attributed in
any degree to the hypertension; on the contrary, the hyperglycemia sometimes
described in cases of hypertension is more probably an indication of pancreatitis
and mild diabetes. This being one of the earlier cases of the series, conservatism
seemed to favor leniency in the treatment. Fuller experience indicates that the
right plan would be to reduce the weight sufficiently to keep the blood sugar nor-
mal. Nevertheless, in view of the mUdness of the case, if the patient follows a
fairly reasonable diet without letting her weight rise too high, she can probably
go through life without further trouble from her diabetes.

CASE NO. 22.

Male, married, age 52 yrs. American Jew; cigar manufacturer. Admitted
Nov. 20, 1914.

Family History. — Father died of pneumonia at 74. Mother, now 74, has kid-
ney trouble. One brother living and well. Two sisters died in childhood, a
third of appendicitis at IS, a fourth is living but has carcinoma of breast. No
tuberculosis, syphilis, or nervous disorders in family. Patient has been married
31 years; wife living and well. Five children; one died of diphtheria in infancy,
four living and well.

Past History. — Practically never sick from childhood up. Neisser infection
twice. Syphilis denied. At age of 21 patient was rejected for life insurance
because of alleged B right's disease. He consulted eminent specialists, and the
slight albuminuria was classified among the earliest examples of orthostatic al-
bimiinuria. For many years he has never been without albumin and casts in
urine, but has had no symptoms other than these and has never had to miss a
single day from business. For part of his life patient drank considerable wine in
connection with business dealings, and smoked IS to 20 cigars a day. He started
as a poor boy and became a millionaire, and has lived at highest nervous tension.

258 CHAPTER III

In the past 10 or 12 years he has had 25 or 30 hysteric attacks in which he was
practically irresponsible. He is accustomed to rich Uving. Bowels constipated.

Present Illness. — 2 years before admission sjrmptoms began with extreme
himger and thirst, loss of weight, bad breath, and cramps in the legs. On ac-
count of failing vision he consulted an oculist, who immediately asked for a
specimen of urine and diagnosed diabetes. The diet since then has been sUghtly
restricted qualitatively, but quantitatively two or three times as much as re-
quired by a normal appetite. The loss of weight has continued nevertheless.

Physical Examination. — ^A shghtly buUt, somewhat emaciated man with pale
complexion and nervous, feeble appearance. Several teeth missing; those pres-
ent show sUght caries and pyorrhea. Throat somewhat congested; left tonsil not
visible, right protrudes slightly. Shght generalized lymph node enlargement.
Heart very shghtly enlarged to left. Arteries palpably sclerosed. Blood pres-
sure 135 systoUc, 110 diastohc. Liver edge 2 cm. below costal margin. Reflexes
normal. Examination otherwise negative. Urine shows shght albumin and
numerous hyahne casts.

Treatment. — The patient's extreme nervousness, as also headaches and ter-
rors at night, required the use of codeine during the early days in the hospital.
He was kept on an observation diet for the first 3 days, poor in carbohydrate, and
particularly with total calories limited to about 1600 on Nov. 21 and 900 on
Nov. 22. The glycosuria was thus greatly diminished. Nevertheless fasting was
instituted as soon as the general condition seemed to permit. Owing to weak-
ness, the patient was in bed during the fast. On Nov. 23 and 28 the fasting
was absolute. On the intervening days whisky was given, but never above 70
cc. Glycosuria ceased with the first day of fasting. With continuance of the
fast, the ferric chloride reaction diminished to traces. On Nov. 29 a carbohy-
drate-free diet of 45 gm. protein and 2080 calories was tolerated without glyco-
suria, but brought back a heavy ferric chloride reaction. On the next day the
diet was diminished to 23 gm. protein and 600 calories. The weakness and
nervousness stiU being salient features and the patient being very hungry, a lib-
eral diet was permitted on the subsequent days, rising by Dec. 19 to 97 gm. pro-
tein, 33 gm. carbohydrate, and 3000 calories. Traces of glycosuria were fre-
quent on this high diet, and well marked ferric chloride reactions continued. By
this time the general condition had improved and the patient had grown more
accustomed to hospital hfe and dietary restrictions. Accordingly, on Dec. 21 a
more rigid treatment of the diabetes was undertaken. On that day the only
food was 50 gm.. alcohol. Green vegetables were gradually added to the alcohol,
representing 7.5 gm. carbohydrate on Dec. 22 and increasing to 107 gm. on Dec.
28. The ferric chloride reaction was still stubborn notwithstanding this car-
bohydrate intake without glycosuria — an illustration that food is not the only
controlling factor. In view of the patient's weakness and irritability a more
Uberal diet was again resumed. He was dismissed on Jan. IS, 1915, on a diet of
approximately 100 gm. protein, 15 gm. carbohydrate, and 2400 calories. The body

CASE RECORDS 259

weight was SO kg. at admission, 47.2 kg. at discharge, the period of treatment thus
representing undernutrition to the extent of a loss of 2.8 kg. weight. There had
been a notable gain in strength, so that the patient was now outdoors daily and
was becoming restless owing to a desire to return to work. The nervousness was
greatly lessened and he felt that hfe was again worth hving. Albuminuria and
casts persisted, but several functional tests during the stay in hospital had shown
a normal index of urea excretion. The patient, being stiU weak, was instructed
not to work more than half of each day and to pay attention to rest and general
hygienic measures.

Subsequent History. — ^The urine continued negative to sugar and ferric chloride
tests, with the usual albumin and casts present. By Feb. 10 the weight had
risen to 53.2 kg. The blood pressure was 153 systoUc. The patient at this time
was working 6 or 7 hours a day, was taking horseback rides and other exercise,
and reported himself free from nervousness, sleeping soundly at night, and en-
joying life. In appearance he was very greatly improved. By Apr. 12 there had
been a further increase of 2 kg. in weight. The blood pressure was 180 systolic,
135 diastohc. He was warned that the gain in weight was contrary to instruc-
tions, and the diet was ordered changed to 115 gra. protein, 20 gm. carbohydrate,
and 1600 calories; i.e., the protein and carbohydrate were slightly increased and
the fat decidedly diminished. This allowance of about 30 calories per kg. was
expected to maintain his nutrition without further increase of weight. On July 7
the patient reported that he had been f eeUng as well as in his earlier years be-
fore the onset of diabetes. Occasional headaches recurred but were reheved by
catharsis. There had been a further sHght increase of weight up to 54.4 kg.
The blood pressure was 195 systolic, 160 diastolic. The patient had departed
sUghtly from diet, particularly by adding bread occasionally, and the urine showed
a trace of glycosuria and a moderate ferric chloride reaction. This trace always
disappeared with a single fast-day, and he was warned to adhere to diet and keep
sugar absent.

Second Admission. — ^The patient made no further report until he reentered the
hospital Jan. 24, 1916, slightly more than a year after discharge. He had car-
ried on his large business continuously and efl&ciently during this time and also
had enjoyed much recreation. He returned with glycosuria again present, in con-
sequence of too many visits to restaurants in the course of his amusements. The
weight was 50.2 kg.; i.e., 0.2 kg. more than at previous admission. He had been
running down lately by reason of his indiscretions in diet, but nevertheless was far
stronger and in better condition in all respects than at his previous admission.
Physical examination practically as before. Blood pressure 200 systohc, 135 dias-
tolic. AU the conditions being more favorable, measures were now instituted for a
radical clearing up of both glycosuria and ketonuria. 4 days of absolute fasting
were imposed (Jan. 28 to 31). This was followed by a carbohydrate period in
the form of the usual tolerance test, i.e. on Feb. 1 green vegetables were given
containing 10 gm. carbohydrate, and this was increased by 10 gm. daily. The

260 CHAPTER rn

traces of glycosuria on Feb. 4 and 5 were accidental in character and disap-
peared with further increase of carbohydrate intake. A tolerance of 150 gm.
carbohydrate was thus demonstrated on Feb. 15. By this time the ferric chloride
was entirely negative, the blood pressure had gradually diminished to 160 sys-
tolic, 120 diastolic, and the patient was feeling well enough to have recovered
from the fears which had brought him back to the hospital. Accordingly at this
point he suddenly announced that urgent business matters required his attention
and that he must leave immediately. He was therefore discharged on the fol-
lowing day with instructions not to return.

Third Admission. — ^Nothing more was heard from him until on Oct. 17, 1916,
his wife telephoned that he had had an attack of apoplexy and was in a critical
condition. He was found in an excessively excited state, with partial right sided
hemiplegia. The body weight was again 50.2 kg.; the blood pressure 190 systolic,
125 diastolic, the blood sugar 0.305 per cent, the CO: capacity of the plasma 81
per cent. Xhe urine showed moderate sugar and negative ferric chloride reac-
tions. He was placed on a diet of 65 gm. protein, 10 gm. carbohydrate, and 1000
calories. On this diet glycosuria diminished to only occasional traces, but the
blood sugar never fell below 0.2 per cent. Only slight glycosuria resulted from
an increase of diet to 65 gm. protein, 35 gm. carbohydrate, and 1600 calories.
Meanwhile, with rest, the paralysis was gradually clearing up. In Dec. and Jan.
it seemed feasible again to undertake thorough treatment of the diabetes. A
week of fasting (Jan. 7 to 13) was well borne. At the end of it the ferric chloride
reaction was negative, the ammonia nitrogen excretion only 0.12 gm., the plasma
bicarbonate 68 per cent, but the blood sugar was stiU 0.222 per cent. A car-
bohydrate test with the usual increase of 10 gm. daily showed a tolerance of
only 30 gm. carbohydrate in the form of green vegetables. Treatment was con-
ducted according to the usual principles, the protein being kept low (50 gm. or
less daily) partly on account of the renal condition. Rigorous imdernutrition
brought the usual results, so that in Feb. a tolerance of 120 gm. carbohydrate
was demonstrated, and the stubborn hyperglycemia was at last reduced, not to
normal, but well below the renal threshold. By Mar. the patient was able to
tolerate 65 gm. protein, 10 gm. carbohydrate, and 1400 calories. His weight had
been reduced to 41 kg.; i.e., a loss of 9.2 kg. The paralysis had gradually di-
minished so that he was able to be about again and to make some use of his
right arm. He was improved sufficiently that he was no longer trustworthy in
regard to diet. He was discharged with the feeling that life could not be greatly
prolonged.

Remarks. — ^The case represents the treatment of diabetes in the presence of
nephritis. It is evident that such a combination presents no obstacle to the
carrying out of the usual method. A diet low in both protein and calories is
beneficial from the standpoint of both the diabetes and the nephritis, and there
is no antagonism in any of the measures required. In this instance the patient
was saved from threatening weakness and nervous collapse connected with his

CASE RECORDS 261

diabetes, and it was possible, as shown especially in the second admission, to
make the urine normal and bring the blood sugar also to a normal level. Disaster
came from the side of the nephritis. The patient is failing but was alive at
last report.

CASE NO. 23.

Male, married, age 44 yrs. American; insurance agent. Admitted Nov. 27,
1914.

Family History. — Father and mother living and well. One sister died in in-
fancy, and a brother of pneumonia. No diabetes or other special disease in
family. Patient married 20 years. Two children, one living and well at 17
years; the other died in a difficult labor. An interesting addition to this history
at time of admission is that patient's mother has since developed diabetes at the
age of 74.

Fast History. — Measles, mumps, and chicken-pox in childhood. Healthy life.
Neisser infection at 19; syphilis denied. 14 years ago had "bloody dysentery"
for a week. Habits regular; moderate drinking and smoking. Appetite normal.

Present Illness. — 9 years ago, after much worry in business, glycosuria was
discovered when patient applied for life insurance. His family physician pre-
scribed diet and pronounced the condition only a transient glycosuria. Subse-
quently life insurance was granted. He has had constant medical supervision
and the tendency to glycosuria has steadily increased, so that during the past 2
years he has never been sugar-free, and the amount has varied from 3 to 7 per
cent. His weight has diminished from 195 to. 165 pounds. He can stUl do con-
siderable work, but 'feels a decided impairment of strength and endurance. No
polyphagia. Urine not more than 3 liters. He avoids sugar and most starches,
but his diet includes oatmeal, two sUces of fraudulent gluten bread, fruits, vege-
tables, and occasionally a potato. He was referred to the Institute by a com-
petent general practitioner because both glycosuria and ketonuria were heavy on
the diet stated. The physician was in the old-time dilemma of hesitating to
increase glycosuria by adding carbohydrate, and fearing to increase acidosis by
withdrawing carbohydrate.

Physical Examination. — Height 172.5 cm. A well developed, adequately
nourished, healthy appearing man. Teeth in good condition. Tonsils slightly
enlarged. Liver edge 3 cm. below costal margin. Examination otherwise
negative.

Treatment. — ^The patient was kept for a week on an observation diet of 95 to
120 gm. protein, 10 to 20 gm. carbohydrate, and 1800 to 2400 calories. The
highest anunonia nitrogen excretion was 2.31 gm. There were no symptoms of
danger or even discomfort. Fasting was begun on Dec. 5, first absolute, then (Dec.
6 and 7) with alcohol up to 52.5 gm. This was followed by a low carbohydrate-
free diet, but glycosuria promptly returned (Dec. 10 to 11) on about 50 gm.
protein and 1600 calories. Ferric chloride reactions persisted, and the ammonia

262 CHAPTER III

excretion was practically as high as at the beginning. The case had been taken as
a mild one. These signs indicated that notwithstanding the absence of striking
symptoms, the real condition was by no means trivial and nothing but radical
undernutrition could bring a satisfactory result. The patient was absolutely
obedient and gave his full confidence, and a rigid program was therefore insti-
tuted. With a view to combating acidosis, food was given chiefly in the form of
alcohol, the highest intake being about 260 cc. whisky on certain days in Feb.
The general plan of treatment is best seen from the graphic chart. Protein-fat
diets were given on a few days, for example, Jan. IS to 17, but for the most part
the diet consisted only of whisky with addition of carbohydrate from time to
time up to the limit of tolerance. This hmit was very low. The giving of 40 to
70 gm. carbohydrate in the form of green vegetables with no other food but
whisky was sufficient to cause glycosuria on repeated occasions in Dec, Jan.,
and Feb. The maximum alcohol doses above mentioned, with the addition of
these quantities of carbohydrate, failed to abolish the persistent, fairly heavy
ferric chloride reactions. Also it was not possible to allow an adequate diet and
await a later recovery of tolerance for clearing up acidosis, because the total food
tolerance remained persistently low. For example, on Jan. 17 a carbohydrate-
free diet of 89 gm. protein and 1790 calories gave rise to glycosuria lasting 2 days.
Under such conditions it is generally necessary to master both the glycosuria and
the acidosis before much real improvement of assimilation can be expected. At
the end of Mar. and first of Apr. the patient's weight touched its lowest point,
51.4 kg.; i.e., a loss of 19.2 kg. during 4 months of severe continuous under-
nutrition. The patient had come to the hospital looking strong and robust.
By this time he appeared thin and weak. His strength was definitely dimin-
ished, and his general decline seemed so evident that only fuU confidence on his
part and on the part of those conducting the treatment permitted the completion
of the necessary program. But about this time the ferric chloride reactions grew
steadily paler, until they were negative in certain urine specimens of each day and
not more than traces in the other periods. Also a recovery of assimilation was
evident, such that on Apr. S to 7 a diet of approximately 100 gm. protein, 20 gm.
carbohydrate, 100 gm. alcohol, and 2200 calories was tolerated without glycosuria.
Exercise had not been employed in the earUer treatment, because of uncertainty as
to its effects in the presence of marked undernutrition and a persistent tendency
to acidosis. It was now begun and rapidly increased up to the hmit of strength.
The high calories in the later diets were permitted in proportion to the amount of
physical labor performed. On Apr. 8 it appeared feasible to discontinue alcohol,
and except for the fast-day on Apr. 11 it was never resumed. On Apr. 9 and 10 the
diet was made approximately 100 gm. protein, 30 gm. carbohydrate, and 1500 cal-
ories. This was increased rapidly to 2700 to 3000 calpries with the same protein
and carbohydrate. A regular fast-day each week diminished the average intake
to about 86 gm. protein and 2300 calories daily, or about 43 calories per kg. for
the weight of approximately 54 kg. at that time.

CASE RECORDS 263

The patient, though thinner, now both felt and looked far better than at ad-
mission. He was up to full strength in every way and able to carry on his regu-
lar business and in addition take much exercise and recreation daily. He was
discharged in this condition on May 8 to spend the summer in the country. He
was instructed to report in 6 weeks and not to gain more than 2 pounds in this
time.

Subsequent History. — In the country he spent his days in walking, riding, swim-
ming, tennis, and other exercise, buUding up strength while keeping weight
within prescribed limits. In Aug. ferric chloride reactions ceased to appear.
The urine never showed sugar except traces on rare occasions when he made
unintentional mistakes in diet. He returned to resume his regular business in the
city in Sept.

On account of persistent hyperglycemia, exercise was increased, the patient
preferring this to a reduction in diet. Daily exercise was taken in the form of
horseback riding, athletic exercises under an instructor, swimming, and boxing.
He also walks to business, an average of about 8 mUes daily, frequently walks
20 or 30 miles on Sundays, and also plays tennis and squash three or four times a
week. His business duties occupy about 5 hours a day, and in the remaining
hours he has made a trained athlete of himself. Because hyperglycemia stiU
persisted, on Dec. 17 the diet was made 130 gm. protein, SO gm. carbohydrate,
and 2500 calories, this change representing particularly an increasd in carbo-
hydrate and a diminution in total calories. At the same time he was allowed to
increase his office work by 1 hour. On New Years day, 1916, the patient added
a large baked potato to his diet without glycosuria, but was warned against a
repetition. Traces of glycosuria appeared in subsequent months on rare occa-
sions, and accordingly on July 10, 1916, the diet was diminished to 130 gm.
protein, 40 gm. carbohydrate, and 2200 calories. In the entire time since then
there was a trace of sugar in the urine only on 2 days. The weight at last report
was 68.4 kg., in comparison with the 70.6 kg. at the time of first beginning treat-
ment in hospital. The general strength and subjective condition are the best
the patient ever enjoyed.

Acidosis. — Though mostly shght, this was notably stubborn, and the mastery
of it was one of the most difficult features of the treatment. The prolonged pro-
gram of undernutrition, with alcohol short of intoxication and carbohydrate to the
point of glycosuria, resulted in a slow decline of the ammonia to a normal level
about the middle of Feb. There was a prompt rise with the addition of small
quantities of protein and fat to the diet late in Feb. and early in Mar., followed
by another slow decline. Also, in addition to the tenaciously persistent ferric
chloride reaction, the CO2 capacity of the plasma indicated the same chronic ten-
dency to acidosis. From the graphic curve it can be seen that the values were
generally near the lower normal limit and frequently fell considerably below this.
Sodium bicarbonate was used twice; namely, SO gm. on 1 day to check the par-
ticularly marked fall of the plasma alkalinity at the close of Feb., and 30 gm.

264 CHAPTER m

daUy on Mar. 8 and 9. These doses gave immediate relief from slight symptoms
of malaise of which the patient complained at this time. But obviously his fun-
damental trouble was not lack of alkali, and the treatment had to be directed
to the causes imderlying the state of acidosis.

At the time of discharge from hospital the ammonia nitrogen excretion was stiU
0.8 to 1.2 gm.; and some color was shown with ferric chloride in certain urine
specimens every day, while specimens in other portions of the day were negative.
As mentioned, the ferric chloride reactions became fully negative in Aug. and
have remained so since. Acidosis has also remained absent by other tests. On
July 25, 1916, the CO2 capacity of the plasma was 60.6 per cent, and it has since
remained high.

Exercise and Blood Sugar. — It seems probable from other experience that no
harm would have been done and progress might have been hastened by using ex-
ercise in this case from the outset. The improved assimilation of carbohydrate
and other food might have aided in a quicker clearing up of acidosis. Exercise
was carried to a higher point in this patient than in any other of the series. As
stated, he has made a trained athlete of himself and has enjoyed the highest
vigor and subjective health. In a general way it seemed evident that exercise
improved his assimilation. Precise experiments concerning the effect of exercise
upon his blood sugar were not performed.

It will be noted in the graphic chart that the blood sugar in the latter part of
Mar. was below 0.15 per cent and fell to normal. With the higher carbohydrate
and higher total diet in Apr. it rose as high as 0.17 per cent, but came down,
apparently as a result of exercise, to a nearly normal level at discharge. After
leaving hospital the patient's weight gradually rose and the blood sugar likewise
increased. On Oct. 6, with weight up to 60.9 kg., the sugar in whole blood was
0.185 per cent, in plasma 0.208 per cent. It was at this point that a maximum of
exercise was begun, the patient preferring this to a reduction of diet. Nevertheless
on Oct. 18 the sugar in the whole blood was 0.192 per cent, in the plasma 0.208
per cent, whUe the patient was feeling in splendid condition. On Oct. 25 the
blood sugar was again 0.192 per cent and the plasma sugar 0.208 per cent; on Oct.
28 the plasma sugar was 0.222 per cent; on Nov. 15 the blood sugar was 0.161 per
cent, plasma sugar 0.222 per cent. Traces of glycosuria had formerly been cleared
up on repeated occasions by exercise, but it seemed evident that the diet was too
high, so that exercise could not lower the hjrperglycemia or entirely prevent re-
currences of these traces of sugar. Accordingly the diet was modified on Dec.
27 as above noted. On July 10, 1916, the blood sugar was 0.156 per cent, the
plasma sugar 0.217 per cent. The weight as above mentioned was higher than
before; namely, 68.4 kg. On July 25 the blood sugar was 0.143 per cent, the
plasma sugar 0.169 per cent. On Aug. 2, 1916, the blood sugar was 0.167 per
cent, the plasma" sugar 0.178 per cent. A reduction of body weight is the one
means which may be expected to control the hyperglycemia. The chief value of
exercise from the standpoint of permanent results probably consists in buming

CASE RECORDS

265

up surplus calories and keeping down excess weight. Exercise has doubtless been
somewhat overdone in this case.

Nitrogen Loss. — In the prolonged period of almost protein-free diet, it is evi-
dent that much protein must have been lost from the body. The nitrogen analy-
ses of the urine are very incomplete. If the known points of the nitrogen output
are joined to make a curve as shown in the graphic chart, a reckoning from such a
curve win give a rough idea of the depletion of body nitrogen. The general
undernutrition is evident from the following table:

Total nitrogen output

Protein intake

Nitrogen "

" deficit (output — intake)

Alcohol calories in diet

Food " " "

Total " " "

77 days.

Per day

(average) .

511.32

gm.

6.61

gm.

1236.20

It

16.10

{{

197.80

tt

2.50

u

313.52

tt

4.14

tt

28979

376

24284

316

53263

692

Alcohol. — Prolonged high dosage of alcohol in this patient was for the purpose
of kpeping up strength by supplying calories and if possible aiding to diminish
acidosis. According to clinical indications it was of value for the first purpose.
There is no evidence that it had any value for the second purpose. If the thing
were to be done over, less alcohol or none would be used. Better and quicker
results could doubtless be obtained by a low protein diet, without fat, with vege-
table periods interspersed. Body nitrogen and strength would be better con-
served by the protein. Alcohol is probably injurious rather than beneficial as
regards acidosis.

Remarks. — ^The outstanding feature of this case is that a patient in seemingly
good physical condition was subjected to over 3 months of continuous under-
nutrition and brought into a thinner and seemingly worse condition as a thera-
peutic measure on the basis of laboratory findings alone. The case was not
mUd as imagined when the patient was admitted. It is believed, on the con-
trary, that trouble was shortly impending. The condition confronted was an
assimilation of carbohydrate or protein so low that glycosuria resulted from a
very low intake, and a mild but very stubborn acidosis. An attempt to give any
considerable quantities of protein and carbohydrate would have resulted in con-
tinuous glycosuria. The use of any considerable quantities of fat would have in-
creased or prolonged the acidosis. Accordingly the only escape lay in undernutri-
tion until this dilemma could be broken. The undernutrition was therefore pushed
to the necessary point without hesitation because of any clinical appearances.
The result was successful as stated, and it is believed that a successful result
could not have been attained on any program overtaxing the patient's tolerance

266 CHAPTER ni

on the side of either carbohydrate or fat. The ultimate outcome has been good
from both the clinical and the laboratory standpoints. The persistent hyper-
glycemia is the one unfavorable feature. Unless it diminishes in the natural
course of improvement under present treatment, a reduction of body weight will
have to be ordered; otherwise there may be downward progress and somebody
may call it spontaneous. With simple precautions now, the situation promises
a favorable outcome of an unexpectedly difficult case.

CASE NO. 24.

Male, married, age 44 yrs. American; manufacturer. Admitted Nov. 28,
1914.

Family History. — Father and mother still ahve. The former has glycosuria,
discovered 4 years ago, but no other symptoms.' A paternal aunt died of cancer.
A brother and a sister of the patient are well. Patient has been married 30 years.
Wife had two miscarriages, then one chUd, who is ahve, aged 19.

Past History.— Healthy hfe, spent in small town in Indiana. Measles and
mumps in childhood. Neisser infection at 19. SyphUis denied. Rheumatism
10 years ago; joints involved successively and very painful; night sweats; illness
lasted about 6 weeks but was not severe enough to confine to bed. Occasional
sore throats before and since this time. 8 years ago patient had indigestion,
with pain after eating, pale feces, and yellowness of skin. This continued about
a year and he lost 25 pounds weight, but finally recovered under forced feeding.
No fever or sharp pain at any time. There is a discharge from the left ear
dating from boyhood. Hearing is much impaired in this ear. No excesses in
alcohol or food. For many years he smoked 6 to 10 cigars daily. Last Mar.
he diminished his smoking to a minimum; has noticed no benefit. Normal
weight is 165 pounds.

Present Illness.— 7 years ago, on account of loss of weight, extra food was
taken and considerable candy eaten. There was no special appetite, and no
thirst or other symptoms, and the food and candy were taken merely with the
idea of putting on weight. His eyesight then began to fail, and he consulted an
ocuUst who examined the urine and diagnosed diabetes. A diet was later pre-
scribed, and on this he regained some weight. Within a year, however, there
was further loss of weight, and polyphagia, polydipsia, and polyuria were pres-
ent. He then spent 10 days in a diabetic sanitarium, and became sugar-free for
the first time in 10 months on carbohydrate-free diet with whisky and sodium
bicarbonate. For the past 5 years he has made annual trips to this sanitarium,
remaining for 10 days to 10 weeks at a time. During the past 3 or 4 years he
has not become sugar-free on these trips. During the past year he was worn out
by nerve strain attendant upon a defalcation and a lawsuit. On the last day
of the trial he had to be carried to court on a cot to testify, and has been bed-fast

'The father refused all dietary restrictions, and died of diabetes in Jan., 1919.

CASE RECORDS 267

for the 2 months since that time. He was brought to this Institute from Indiana
with his physician in attendance, and had to be wheeled or carried.

Physical Examination. — Height 173 cm. A well developed, extremely emaci-
ated man, showing evidence of profound weakness but no acute distress. Teeth
in good condition. Throat congested. Slight enlargement of lymph nodes in
left axilla and groins. Knee jerks sluggish. Routine examination otherwise nega-
tive. The most striking feature aside from the emaciation is a lemon yellow color
of the skin, most pronounced on the face, but noticeable also over most of the
body; the conjunctivae are bluish white and not jaundiced, and the urine is
free from bile. The color suggests pernicious anemia. Blood examination
showed hemoglobin 80 per cent, red cells 4,000,000, leucocytes 6,000, with normal
differential count. Lipemia of heaviest degree present; plasma hke cream. Was-
sermann negative. Urine free from albumin and casts. Blood pressure only 70
systolic, diastolic doubtful at about SS.

Treatment. — Because of the extreme weakness and the absence of threatening
acidosis, the patient was given for 2 days a diet Hke that to which he had been
accustomed; i.e., on Nov. 28 and 29 about 100 gm. protein, 20 to 30 gm. carbohy-
drate, and 2000 to 2100 calories. On Nov. 29 he excreted 45 gm. sugar and 2.5
gm. ammonia nitrogen; on Nov. 30 (the first fast-day), 20.5 gm. sugar and 2.78
gm. ammonia nitrogen. Fasting was begun on Nov. 30, with some misgivings on
account of weakness. Because of tendency to nausea only 30 gm. alcohol were
given the first day, increased to 70 gm. by Dec. 5. Glycosuria was absent by
Dec. 5, and the ammonia nitrogen had diminished to 0.88 gm. (total N output
3.83 gm.). The ferric chloride reaction was much diminished but still well
marked, and the blood plasma was still intensely lipemic. The patient's strength
showed no dechne whatever on account of the fasting, and possibly a slight im-
provement. He was able to sit up in bed to read, and could walk to the bath-
room with assistance. The fasting was therefore prolonged through Dec. 6,
making 6 days. On Dec. 7, one egg, 10 gm. butter, and 500 gm. thrice cooked
vegetables were added to the whisky. This was increased daily, so that on Dec.
10 the intake was 52 gm. protein and 1450 calories. On this diet a glycosuria
of 9.9 gm. appeared. A fast-day with 100 cc. whisky on Dec. 12 failed to clear
up the glycosuria. Only one egg and 20 gm. butter were added to the whisky
on Dec. 13, yet glycosuria persisted. On Dec. 14, another fast-day with 140
cc. whisky cleared up the sugar and the ferric chloride reactions. On Dec. 15, a
diet of only 17 gm. protein and 600 calories (450 of which were alcohol) caused
glycosuria of 2.61 gm., this sugar being doubtless partly attributable to the 1000
gm. thrice cooked vegetables allowed for the sake of bulk. This glycosuria per-
sisted under similar conditions on Dec. 16, so that a fast-day with 140 cc. whisky
became necessary on Dec. 17. . Beginning Dec. 18, all vegetables were omitted
in the attempt to build up strength. A diet was given on Dec. 18 and 19 of 52
gm. protein in the form of eggs, 420 calories of alcohol, and olive oil to bring the
total calories up to 2600. The ammonia excretion rose, and persistent traces of
glycosuria appeared. The diet was sharply reduced, so that on Dec. 21 it con-

268 CHAPTER III

sisted of only two eggs and 130 cc. whisky. The eggs were increased until on
Dec. 26 seven were given. Though such diets were frequently below 1000 cal-
ories and composed largely of alcohol, traces of glycosuria remained persistent.
It became established during this time that the patient could not tolerate even
the carbohydrate of 200 gm. thrice boiled vegetables such as celery or Brussels
sprouts, and the protein of six or seven eggs also sufficed to cause glycosuria.
Under such circumstances the prospects for nourishing a patient already seri-
ously weak seemed hopeless. But the notable feature was that the patient's
strength and spirits continually improved during the time when he should theo-
retically have been starving. He became able to sit up in a chair, but was con-
fined to bed almost continuously under orders.

On Jan. 5, 50 cc. whisky, 200 gm. thrice boiled celery, and 100 gm. thrice
boiled asparagus were taken without glycosuria. On Jan. 6, meat and bacon were
added, and the diet was 20 gm. protein, 600 gm. thrice boiled vegetables, and 480
calories. This was tolerated, but on the next day (Jan. 7) 36 gm. protein and
900 calories with only 400 gm. thrice boiled vegetables (celery, spinach, and Brus-
sels sprouts) caused glycosuria. Diets of this sort or lower were continued, with
almost continuous slight glycosuria. The carbohydrate intake shown by the
graphic chart Jan. 21 to 28 was in the form of caramel, which was tolerated in
quantities of IS to 30 gm. daily without glycosuria. Under these low diets the
body weight gradually fell, while the strength slightly increased and the ferric
chloride reactions became pale or negative. With the progressive improvement
it became possible early in Feb. to raise the diet to approximately 68 gm. pro-
tein and 1400 calories, 250 of these being alcohol calories. In the latter part of
Feb. the intake could be markedly increased, and in Mar. and Apr. the diet ran
as high as 80 to 90 gm. protein and 2500 calories (of which 250 were alcohol)
and 200 to 300 gm. thrice cooked vegetables. With this there was a fast-day
weekly. During Feb. the patient was allowed out of bed, and in Mar. he was
encouraged to make trips from the hospital for exercise. On Mar. 12, he was
able for the first time to walk a mile. Thereafter he took steadily increasing
exercise, and high diets were allowed not only to build up strength but also to
support muscular activity. Glycosuria was limited to bare traces demonstrable
only in certain fractional specimens of certain days and not in the mixed 24
hour urine. But at the beginning of Apr. a more definite glycosuria appeared,
also the blood sugar on Apr. 3 was 0.27 per cent. Accordingly food was stopped,
making the diet on this day less than 900 calories. On Apr. 4 only 130 cc. whisky
were given, and on the following days only whisky and soup. After these 3
days of practical fasting, the blood sugar was down to 0.1 per cent.

Then on Apr. 7, 5 gm. carbohydrate were given in the form of green vege-
tables, and these without other food were increased on the following days, until
50 gm. carbohydrate were taken without glycosuria (Apr. 10). On Apr. 12, the
high protein-fat diets with weekly fast-days were resumed, with resultant hyper-
glycemia, so that on Apr. 28 the blood sugar was 0.31 per cent. Accordingly 4

CASE RECORDS 269

days of absolute fasting were imposed, followed by a carbohydrate tolerance test
in regular form. The tolerance was found to be almost 100 gm. carbohydrate.
Up to May 20 diets were given below 1500 calories, containing 10 to 15 gm. car-
bohydrate. Then, because of glycosuria and hyperglycemia, carbohydrate was
omitted, but resumed again in June. By this time the patient could tolerate a
daily ration up to 80 gm. protein, 20 gm. carbohydrate, and 2000 calories, with
an absolute fast-day each Sunday. He was dismissed on such a diet, with the
carbohydrate diminished to 15 gm. The urine was normal, and the clinical
condition, aside from the emaciation, was good.

Acidosis. — The excretion of as much as 2.75 gm. ammonia nitrogen at first in-
dicated a rather marked acidosis, but dangerous symptoms were never present.
An intense ferric chloride reaction was present, and there was the usual odor of
the breath, but no dyspnea. As shown in the graphic chart, t|he ammonia rap-
idly fell during the initial fast. On Dec. 8 the ammonia nitrogen was 0.74 gm.
and the ferric chloride reaction was negative. Protein-fat diet, together with
the use of whisky, sent the ammonia nitrogen up to 1.68 gm. on Dec. 11. It
then fell promptly when the diet was reduced, and beginning Dec. 18 rose still
higher as the diet was made higher than before, reaching the summit on Dec. 21.
It again fell with reduction of diet, and even on the large carbohydrate-free diets
of Mar. and Apr. never returned to the former height. The ferric chloride reac-
tion became consistently negative in the period Jan. IS to 28. Many of the
traces indicated elsewhere were only tinges of color in individual fractions of the
24 hour specimens. For the sake of improvement ia strength, the above men-
tioned high diets of Mar. and Apr. were continued in spite of the well marked
ferric chloride reactions which they produced, with the idea that as long as the
tolerance was rising and the urine kept sugar-free, the mUd acidosis could be left
for disposal in the future. The curve of the blood bicarbonate, beginning Jan. 24,
also reveals the slight chronic acidosis. Alkali was seldom used. 15 gm. sodium
bicarbonate were given on the day of admission; also, toward the close of the initial
fast, 15 gm. on Dec. 2 and 3, and 5 gm. on Dec. 4, all as precautionary measures.
On Feb. 19, 10 gm. bicarbonate left the urine slightly acid. On Feb. 20, 20 gm.
turned the urine alkaline. Likewise the carbon dioxide capacity of the plasma
rose within the lower normal limit on Feb. 20 for the first time. It was still
approximately at this level on Feb. 22, following the fast-day of Feb. 21. But
then, because of the high fat diet or merely loss of the administered alkali, it fell
steeply to the lowest value yet observed; namely, 40 per cent on Feb. 24. It
promptly rose agaui on Feb. 25 without the use of alkali, and the tendency now
to remain closer to the normal level may be interpreted as one indication of the
general improvement. The fasting and minimal diets Apr. 3 to 11 brought
another sharp fall, but thereafter on Apr. 15 it rose still higher than before.
Again the fasting of Apr. 29 to May 2 brought another sharp drop below normal,
followed by a rising tendency; so that on a moderate total diet containing a small
quantity of carbohydrate the blood alkalinity at the last determination on June

270 CHAPTER in

24 was fully normal and higher than at any point in the entire previous record.
Correspondingly the ammonia output was within normal limits, and the ferric
chloride reaction in the urine had become consistently negative.

Alcohol. — ^Whisky was given in moderate quantities for the sake of keeping up
strength. It seemed clearly beneficial for this purpose. The patient felt less
well with larger doses, and it was never pushed to any high quantity. There is no
evidence of any effect ia clearing up acidosis. After Apr. 7 alcohol was (as in
all cases when possible) discontinued altogether. The clearing up of the acidosis
progressed uniaterruptedly, so that the impression is created that the alcohol
was without influence in this regard.

Blood Sugar. — A solitary determination on Jan. 25 showed a strictly normal
value of 0.1 per cent. No fiulher analyses were made until Apr. 1, when the
level was 0.145 per cent. The diets had been high, and at this time were raised
to the maximum; namely, almost 3000 calories on Apr. 2. The result was glyco-
suria, with hjrperglycemia of 0.27 per cent on Apr. 3. The subsequent 3 days
of fasting and alcohol brought the blood sugar down to 0.1 per cent on Apr. 6.
On Apr. 8, with carbohydrate feeding, it rose promptly to 0.182 per cent without
glycosuria. On the ensuing carbohydrate-free diet of 2200 to 2S00 calories it
rose steadily higher, up to 0.312 per cent on Apr. 28. 4 days of fasting restored
a normal value of 0.118 per cent in the plasma on May 3. It will be noticed
that in these periods of feeding and fasting the rise and fall of the blood sugar
and body weight were parallel. A small amoimt of carbohydrate in the diet
from May 11 onward was in excess of the true tolerance, as indicated by the rising
blood sugar, which reached 0.20 per cent on May 18; and though it still rose to
0.232 per cent on May 22, the omission of carbohydrate and a fast-day on May
23 brought a fall to 0.138 per cent on May 24. With restoration of carbohydrate
in the diet the blood sugar again rose, reaching 0.2 per cent on Jime IS. In gen-
eral, it is seen that the hyperglycemia is a more delicate index of the tolerance
than the glycosuria. On the other hand, it is by no means a sole criterion of the
condition or progress. The normal blood sugar of Jan. 25 was the result of 2
months of semistarvation. At later periods the blood sugar was higher, though
the patient's diabetes was definitely improved, in the sense that he could tolerate
more of all classes of food and more easily remain free from both glycosuria and
ketonuria. In other words, an identical diet would doubtless have caused greater
hyperglycemia in Jan. than in June. The hyperglycemia at the time of discharge
was the one noticeably abnormal feature in the condition, but, as the subsequent
experience showed, it could be borne by such a patient without preventing the
general tendency to improvement under treatment.

Body Weight. — ^The patient, whose normal weight was 75 kg., entered weighing
44.2 kg., i.e., 59 per cent of his normal weight, or a loss of 30.4 kg. During
fasting his weight rose by water retention, the sodium bicarbonate of Dec. 2 and
3 probably being responsible for the summit of the weight curve on Dec. 3. The
rise of weight was accompanied by well marked edema of the ankles. The patient

CASE EECOEDS

271

stated it had been present at former times to a still greater extent. With the
continuous undernutrition there was a sUght progressive fall in weight, the lowest
point being 39.8 kg. on Feb. S. Thereafter with the increased diets the weight
steadily rose, so that the patient was discharged on June 28 at precisely his
entrance weight of 44.2 kg.

Nutrition. — ^The salient feature is the degree of undernutrition imposed upon a
patient already extremely emaciated and weak. The patient himself had not
expected to hve. Notwithstanding this state of weakness, he not only with-
stood a 6 day fast successfully, but also bore 2 months of radical undernutrition
thereafter.

From Nov. 30 to Feb. 2 the following calculation can be made.

65 days.

Per day
(average).

Per day
per kg.*

1655.8 gm.
264.9 "
23362
28249
51611

25.40 gm.
4.07 "
359.4
434.6
794.0

5.80 gm.
0.09 "
8.00

Total nitrogen in diet

Alcohol calories

Food "

10.00

Total "

18.00

* On 44 kg. weight.

The case at first seemed hopeless, with the combination of emaciation and
weakness on the one hand and inabUity to tolerate a living diet on the
other. The extreme restrictions necessary for controlling the diabetes were
rigidly carried out, and the unmistakable gain in strength along with loss of
weight under these conditions was the most surprising feature. At dismissal,
with the identical body weight as at entrance, the physical condition was trans-
formed. The man had come as a helpless bedridden invahd supposedly at the
point of death. At discharge he was stiU very thin, and strangers regarded him
as having tuberculosis or cancer, but he was able to make the trip to his home
unattended and carry his two heavy suitcases without assistance.

Subsequent History. — ^The patient resumed his business duties and also took con-
siderable daily exercise as instructed, chiefly in the form of walking. He remained
free from glycosuria and other symptoms, with continuous improvement in
strength and health, untU he committed a few minor indiscretions in diet, con-
sisting only in the addition of a few eggs and vegetables beyond the prescribed
quantity. Persistent glycosuria resulted, which did not stop on omitting aU
carbohydrate or on the routuie fast-days. He reported his condition promptly
and was advised to return to the hospital.

Second Admission. — ^The patient returned Oct. 17, 1915, weighing 45.2 kg.;
i.e., a gain of 1 kg. The glycosuria and ketonuria on his regular diet were both
rather heavy. The ammonia nitrogen was up to 1.54 gm. The carbon dioxide
capacity of the plasma was as low as 46 per cent, and the plasma sugar was 0.35
per cent. But the physical strength was still as good as at discharge, and the

272 CHAPTER in

task of treatment was far easier than before. Blood pressure 102 systolic, 82
diastolic.

After 1 week of observation on the diet which had been tolerated at the former
discharge, fasting was imposed Oct. 24 to 31. The urine was sugar-free on Oct.
30. On Nov. 1, 10 gm. carbohydrate were given in the form of green vegetables,
followed by the usual increase of 10 gm. daily, and definite glycosuria appeared
with 40 gm. carbohydrate. This may be compared with the 100 gm. tolerance
in the previous May and with the zero tolerance at the outset of treatment.

Beguming Nov. 8, a diet of 75 gm. protein, 5 gm. carbohydrate, and 1800
calories caused glycosuria. Therefore carbohydrate was omitted, and the protein
diminished to 50 gm., and total calories to 1300. This diet represented approxi-
mately 1.1 gm. protein and 30 calories per kg., but the weekly fast-days brought
the average down to approximately 0.9 gm. protein and 26 calories per kg. — a
low diet especially in view of the rather vigorous exercise which the patient was
encouraged to take. Nevertheless, the blood sugar remained unduly high and
traces of glycosuria were frequent.

Beginning Nov. 25, an attempt was made to mcrease protein while keeping
the total calories the same by subtracting an equivalent of fat. The protein was
thus gradually raised to 110 gm. on Nov. 30, the calories remaining 1300. The
blood sugar rose markedly, and glycosuria appeared with 100 gm. protein on
Nov. 29.

Beginning Dec. 12, radical undernutrition was maintained imtil Jan. 7 in
the most favorable manner possible, namely by restriction or almost complete
exclusion of fat. The protein was at first kept unchanged at SO gm. On Christ-
mas day as a special indulgence, 85 gm. protein were granted to allow the patient
to enjoy turkey. After Jan. 28 the regular protein allowance was 60 gm. Owing
to exclusion of fat, the total calories were only 300 daily up to Dec. 17. For the
week of Dec. 20 they were increased to 600 by addition of alcohol. By increase
of protein and fat they were brought up to 1000 on Jan. 3 to 6. The most strik-
ing effect of the exclusion of fat was not upon the ammonia but upon the blood
sugar, which was brought well within the normal limits. Also the tolerance was
improved, so that beginning Jan. 8 the patient was able to tolerate a diet of 70
gm. protein, IS gm. carbohydrate, and 1900 calories. The body weight was
down to 43.2 kg., or 1 kg. less than at the former discharge, but the strength
and general condition were better than at any former time. The patient was
discharged on Jan. 18 to resume his business in his home town.

Acidosis.— As mentioned, the ammonia output and carbon dioxide capacity of
the plasma indicated a slight acidosis on admission. The high point of the am-
monia nitrogen at 2.5 gm. on Oct. 26 does not necessarily mean that the ammonia
rose on fastmg. The only previous determinations had been on Oct. 17 to 18,
and it is possible that toward the close of the week of feeding the ammonia was
higher than on Oct. 26. After this date the ammonia fell sharply, and reached
a still lower point with the carbohydrate tolerance test on Nov. 3. With protein-

CASE RECORDS 273

fat diet it again shot up to 2.5 gm. N on Nov. 11. On Nov. 15, following a
fast-day, it was again found at the lower level of 0.7 gm., rising again with pro-
tein-fat diet. But as this diet was only 1300 calories, the ammonia remained de-
cidedly lower than it had been with 1800 calories. Thereafter the curve slopes
gradually down to the normal output of 0.35 gm. at discharge. The ferric chlo-
ride reactions were easily cleared up and remained negative. The carbon dioxide
capacity rose with fasting to the lower normal limit on Oct. 30. With a slight
fluctuation it came safely up within normal values with the carbohydrate tol-
erance test on Nov. 5. With the 1800 calory diet composed chiefly of fat, it fell
steeply below the lower normal level on Nov. 10. Thereafter it fluctuated above
and below the lower normal limit. The highest value, namely 71.6 per cent,
was shown on the fast-day of Dec. 12. At discharge it was exactly at the lower
normal limit of 55 per cent.

Blood Sugar. — ^At admission the plasma sugar was 0.35 per cent, and with con-
tinuance of observation diet reached 0.43 per cent on Oct. 21, and 0.44 per cent
on Oct. 22. It fell sharply on fasting, so that on the second fast-day (Oct. 25)
it was down to 0.17 per cent. The succeeding fluctuations are not explained.
The behavior for several days is so bizarre that the accuracy of some analyses is
called into question. But on Oct. 29, the day when glycosuria ceased, the
plasma sugar had fallen to 0.23 per cent. With the carbohydrate tolerance test
it rose to 0.325 per cent on Nov. 4. On Nov. 8, following the fast-day of Nov. 7,
it was down to 0.2 per cent. The diiet of 1800 calories caused a rise to 0.44 per
cent on Nov. 11. Thereafter, with the diet of 1300 calories, it wiU be seen that
the sugar tended to be up during the week and down on the morning after the
weekly fast-day, but hyperglycemia was continuous. The rigorous undernu-
trition beginning Dec. 12 was what definitely brought the blood sugar down
within normal limits. On the hberal diet with 15 gm. carbohydrate at discharge, '
hyperglycemia again resulted to the extent of 0.16 per cent plasma sugar. This
was the one unfavorable feature at discharge.

Exercise. — Beginning Nov. 11, the patient was exercised daily to the point of
exhaustion, being required to walk up and down 8 flights of stairs 6 times daily,
walk 3 or 4 miles, and toss a 6 pound medicine ball for half an hour daily. With
this amount of labor the diet of 1300 calories was definite undernutrition, yet
neither the body weight nor the blood sugar diminished very perceptibly. The
clinical condition was rather unfavorably affected, however, and the patient was
tired and exhausted from the prolonged exertions. Therefore, beginning Dec. 12,
he was kept in bed during the period of marked undernutrition, and gained in
well-being by reason of the rest. With the higher diets which began in Jan.
he was allowed to take moderate exercise, and was advised to continue this at
home. -

Subsequent History. — ^The patient remained at home from Jan. 18, 1916, to
June 25, 1917, and during this time missed only 6 days from his regular busi-
ness, in consequence of slight additions to the diet, or on two occasions because

274 CHAPTER m

of colds. The weight was up to 48.1 kg. One of the colds mentioned then caused
a setback requiring slight reduction of diet, so that during the summer the
weight was approximately 46 kg. On Jan. 13, 1917, at the patient's request,
he was allowed to diminish his diet from 1900 to 1500 calories, which he said
satisfied him, and on this basis he omitted the weekly fast-days. On May 31,
1917, a telegram was received from the patient stating that he had yielded to a
holiday temptation to eat strawberry shortcake and pie, and was showing heavy
glycosuria in consequence. He was instructed to fast himself sugar-free, and
did so successfully. On June 13, he accidentally increased his diet by 300 calories,
and showed a trace of sugar in consequence.

Third Admission. — On June 25, he appeared unexpectedly at the hospital,
stating that he had decided to travel for a change, and had dropped in to report,
and to stay for examination if desired, especially as he was now finding trouble in
remaining sugar-free after his recent indiscretions. The weight was 45.5 kg.
Although slight glycosuria and ketonuria were found present, the condition was
now very simple from the therapeutic standpoint, and the opportunity was em-
ployed to carry out a test of the effect of fat feeding, as described in Chapter VI.

Remarks. — The heavy Upemia which was such a striking feature of this case at
the outset would have been an interesting feature to study chemically if
circumstances had permitted. Presumably it was responsible for the remark-
able yellow color of the patient, but this color persisted with Uttle diminution
long after the blood plasma had become entirely clear. This color of the skin
was very well marked at the second admission. By the third admission it had
almost entirely disappeared and the complexion had begun to look normal.

Also, though the weight was only 1.3 kg. more than at the original admis-
sion, the face and bearing were different. The patient was stiU excessively
thin, but with the change in facial expression, complexion, and energy of move-
ment, strangers no longer looked upon him as a sick man, and he behaved in all
respects like a normal person. The outcome is therefore a satisfactory one un-
der the circumstances. The diabetes seems to be under control, and any mani-
festations appearing can in each instance be cleared up more easily and quickly
than on former occasions — one indication of favorable progress. The diabetes
was genuinely severe, as demonstrated by the prolonged mtolerance of food and
by the enture history. The heavy hpemia may probably be included among the
symptoms of severity. Death must have resulted within a brief period in the
absence of radical treatment. The ultunate prognosis in a case at this age is
generally better than in younger persons, and the tendency to improvement
seems more permanent and genuine.

This patient furnishes another example of the absence of any perceptible
spontaneous aggravation in a very severe case of diabetes under observation for
2i years; but the possibility of downward progress due .to chronic pancreatitis may
yet have to be considered. The patient describes himself as feeling better than
for many years past. He carries on his work successfully and enjoys life. Fur-

CASE RECORDS 275

thermore, he has had no more attacks of cold and grippe than at periods before
his diabetes, and no greater difficulty in recovering from them. Notwithstanding
the still low tolerance, the outlook at the present time appears favorable for some
time to come.

CASE NO. 25.

Female, married, age SO yrs. Austrian Jew; housewife. Admitted Nov. 28,
1914.

Family History. — Parents lived to old age. Four brothers and two sisters are
well. No heritable disease in family. Patient has been married 28 years. Had
six children and later three miscarriages. One child died of diphtheria, another
in an accident; the other four are well, aged 13 to 26 years.

Past History. — ^Healthy life. Patient came to United States from Austria at
age of 28 and has lived in fairly hygienic surroundings. Erysipelas, in 1912
and again in Jan., 1914, was practically the only infection. Venereal disease
denied, although 3 years ago a general eruption is said to have appeared over the
whole body and disappeared after a few days. 8 or 9 years ago, left-sided hemi-
plegia occurred suddenly and improved gradually within 6 months. A second
stroke occurred in Jan., 1914. Edema of ankles has been noticed during past 2
years. Habits have been regular. No alcohol or other special indulgence.

Present Illness. — 3 years ago a routine urine examination revealed sugar.
Since then one test every month has always shown sugar but never acetone. For
2 years past there has been dyspnea and palpitation on slight exertion, so that
she has been practically confined to her house. Dyspnea also has frequently
made her unable to sleep lying down at night, so that she has had to stay in a
chair. No polyphagia, polydipsia, or polyuria. She has been on a lax anti-
diabetic diet of protein, fat, and green vegetables unrestricted in quantity, and
two roUs and a slice of bread daily. Weight 3 years ago 211 poimds, now 186
pounds. 1 week ago the patient went to a hospital clinic, and was ordered to
stop carbohydrate. Thereafter she began steadily to feel worse and has shown
a progressively increasing stupor during the past few days, with nausea which
has led to vomiting during the past 2 days.

Physical Examination. — A large framed, obese woman lying in bed in a stu-
porous condition and irrational when roused. The odor of the breath is partly
sweetish, partly foul. Some dyspnea is present, but seems of a panting and ner-
vous type rather than Kussmaul air-hunger. The face is sHghtly edematous and
pits on pressure. Exophthalmos and apparent photophobia. Pupils react to
light and accommodation. No jaundice. Pyorrhea and receding gums. Tonsils
slightly enlarged. Signs of slight left-sided paresis. Thyroid lobes hard and
definitely palpable; isthmus not felt. Lymph nodes not enlarged. Some bron-
chitis and emphysema. Cardiac dulness extends 4 cm. to right of midstemal
line and 13 cm. to left in fifth interspace. Soft systoHc blowing murmur at apex.
Aortic second sound markedly accentuated. Walls of radial arteries not pal-
pable. Abdomen obese and flaccid, negative to examination. Knee and Achilles

CASE RECORDS 277

On Dec. 9, this was increased to two eggs and 20 gm. butter; and though no
vegetables or other sources of carbohydrate were given, a trace of glycosuria
appeared, and continued when one egg was given on Dec. 10 and two eggs on
the subsequent days. The protein intake ranged from 15 to 46 gm. and the
total calories averaged well below 1000, even including alcohol, until on Dec.
17 and 18 a diet of eggs and olive oil was given, without vegetables or whisky, rep-
resenting 44 to SO gm. protein and 1900 to 2000 calories. Such diets sufficed to
maintain a continuous glycosuria. This cleared up when nothing but two eggs
was given on Dec. 20. But on Dec. 21, the feeding of only 80 gm. asparagus,
containing 2.2 gm. carbohydrate, caused a trace of glycosuria. To clear this up
3 fast-days with whisky were necessary, on Dec. 24 to 26. Then, on Dec. 27,
the feeding of two eggs and 500 gm. thrice boiled vegetables brought back a
decided trace of glycosuria. After omission of all vegetables, the frequent traces
of glycosuria still continued on low diets Umited to eggs, olive oU, soup, and
coffee, none of these diets containing more than 52 gm. protein and 1300 to 1950
calories. The subsequent treatment represented a continuance of such under-
nutrition. The principle was adopted of giving protein to conserve body nitro-
gen and alcohol to assist weakness, while keeping fat and calories at a very low
figure and compelling the patient to burn off her body fat.

She remained almost without appetite, and on Feb. 4 mentioned being hungry
for the first time. The ferric chloride reaction was much diminished and the
occasional traces of sugar were only very faint reactions in fractional specimens
on certain days. The patient was desirous of continuing treatment at home, and
as all immediate danger was over and the one necessity was merely a continuance
of undernutrition, she was allowed to go out on a diet of 1250 calories, 350 of which
were alcohol. She was instructed to take a fast-day whenever sugar appeared and
once every 2 weeks if it did not appear. She was also warned against constipa-
tion and was encouraged to take exercise. At the time of discharge she was be-
ginning to take short walks, which tired her considerably. Aside from the
weakness, symptoms were absent and she felt well.

Second Admission. — Feb. 11, 1915. The patient was readmitted 5 days after
discharge. She had followed her diet but had had no bowel movement during
this time. The former symptoms recurred in milder form, and she was drowsy and
vomiting occasionally when received. The glycosuria was 0.6 per cent, and the
ferric chloride reaction was heavier than at discharge. A low ammonia value
was found on Feb. 13 after 3 days of fasting. There was no albuminuria, but the
face and ankles were again puffy and pitted on pressure. Blood pressure 170
systolic, 110 diastolic. 30 gm. sodium bicarbonate may have played a part in
the edema. The treatment was carried out on the same lines as before, the
most important feature being the purgation with 2 gm. compound jalap powder
daUy, which yielded the same enormous stools as before. The first 12 days in
hospital, up to Feb. 23, represented almost continuous fasting. 200 calories of
alcohol were given almost daily during this entire period in hospital. The acute

278 CHAPTER ni

sj^nptoms passed off easUy. The food tolerance was obviously higher than be-
fore, and a more liberal diet was gradually built up, finally reaching 83 gm. pro-
tein and 2000 calories at the time of discharge on Mar. 25. Traces of glycosuria
were frequent but easily controDed. Albuminuria was constantly present after
the initial days. The blood pressure on Feb. 16 was 205 systolic, 130 diastolic;
on Feb. 20, 185 systoKc, 140 diastolic. The patient was feeling stronger and in
better condition in aU respects than at the former discharge. The diet pre-
scribed to be followed at home was carbohydrate-free, containing 100 gm. pro-
tern (1.5 gm. per kg.) and 1500 to 1750 calories (23 to 26 calories per kg.). It
was considered probable that she could remain free from glycosuria on this diet,
and if so the shght persisting ketonuria would gradually take care of itself.

Subsequent History. — Reports showed that the patient remained sugar-free
and continued to gain in strength and well-being at home. On May 21, her son
telephoned that she had had some sort of stroke during the night and an ambu-
lance surgeon had diagnosed pulmonary edema. Her death occurred the same
day, and the certificate of the coroner's physician assigned chronic nephritis as
the cause. There was no sugar in the urine at any time.

Acidosis. — The acidosis was never quantitatively high, and the coma was
atypical in character. There was the familiar history of onset shortly after
exclusion of carbohydrate from the diet, but constipation seemed to be a more
important factor. More complete analyses of blood and urine would have been
valuable had they been possible at this time. Along with the general food in-
tolerance, the ammonia nitrogen was slow in reaching normal limits, but at the
first discharge was down to about 0.56 gm. At the second admission the figure
0.28 gm. ammonia nitrogen was obtained after 3 days of fasting; there might weU
have been a much higher ammonia earlier in the attack. Such a possibility is
strengthened by the rise to almost 2 gm. ammonia nitrogen with the diet of only
1100 calories on Feb. 26. The ferric chloride reaction became pale toward the
close of each stay in hospital, and accordingly no further attention was paid to
it, since with continuance of undernutrition and freedom from glycosuria it was
certain to become negative.

Estimations of the carbon dioxide capacity of the plasma were made begin-
ning Feb. 23, and confirmed the tendency to chronic acidosis. Inasmuch as so-
dium bicarbonate had been used rather liberally in the opening days of each
hospital period and had presiamably raised the blood alkalinity, there is some
ground for supposing that such analyses if made during the stuporous attacks
would have indicated a true acidosis coma. Subsequently, in the absence of
bicarbonate, the carbon dioxide capacity of the plasma in Feb. and Mar. ranged
between 45 and 53 per cent. There is no evidence that alkali dosage would
have altered the subjective condition, which was good; and the fundamental acido-
sis process could be influenced only by continuance of the undernutrition pro-
gram as adopted, whereas the giving of alkaU would only have masked the lab-
oratory indications.

CASE RECORDS

279

Blood Sugar. — Only one determination was made. This was 0.118 per cent
before breakfast on Mar. 22. There is no evidence of a renal glycosuria, but on
the other hand a continuous h)Tperglycemia seems excluded, notwithstanding
both diabetes and nephritis.

Undernutrition. — During the initial fast, Nov. 29 to Dec. 7, inclusive, the
patient lost 94.3 gm. nitrogen in the urine. Dec. 8 to 11 the ingestion of 7.5 to
15 gm. protein daily left the nitrogen output at its minimal fasting level of about
8 gm. daily. The degree of undernutrition in the first period in hospital is shown
by the following calculations:

Total nitrogen output

Protein intake

Nitrogen " (protein -^ 6.25).
" deficit (output— intake)

13 days.

127.19 gm.
46.70 "
10.35 "
116.84 "

Per day
(average).

9,78
2.60
0.79
8.99

70 days.

Per day
(average).

Alcohol calories . ....

18518
25701
54219

264.5

Food "

495 7

Total "

760 2

Owing to the clinical condition it was not feasible to weigh the patient uritU
Dec. 6, when the weight was 76 kg. The obesity was diminished as rapidly as
feasible by undernutrition, while the body nitrogen was protected as far as pos-
sible by allowing protein in quantities just short of producing any considerable
glycosuria. Fat was the element which was mainly eliminated from the diet,
and general undernutrition and the burning off of body fat was regarded as the
most important therapeutic measure. At the first discharge the weight was 68.4
kg., and at the second admission and discharge respectively it was approximately
66 kg.; i.e., 10 kg. below the first weight. Strength, well-being, and food toler-
ance had risen in proportion to the fall in weight.

Remarks. — The importance of emptying the bowels when there is impending
coma, especially in certain cases, has been pointed out by former writers. In
this instance it seemed the most important therapeutic measure. Though there
were chemical indications of acidosis as above noted, the urine was easily
made alkaline and the actual quantity of acid formed was evidently not great.
A feature of therapeutic interest is the fact that a very obese patient already
suffering from acidosis with nausea and vomiting came through safely with
simple fasting. There is no evidence of any specific value of the alcohol used.
The danger of increased acidosis from fasting in patients of this type is obviously
to be borne in mind; but a coma which comes on with feeding can generally be
treated by fasting. The reduction of the excessive body weight was beneficial

280 CHAPTER ni

from every standpoint. Judging by the threatened coma and subsequent almost
complete intolerance of food, the case might be called extremely severe, but with
mere continuance of undernutrition sufficient to bring the excessive weight
down to normal or slightly below the average normal, the condition would almost
certainly have stood revealed in its true light as one of fairly mUd diabetes. For
this reason, with falling body weight and rising general health, the traces of
glycosuria and ketonuria were ignored to an extent never ventured in younger
patients. Also this patient's nephritis was far more dangerous to her than her
diabetes. The existence of nephritis in no way interfered with the treatment of
the diabetes. Though the blood pressure diminished as the ordinary conse-
quence of hospital care, there is no indication that the nephritis was improved
by the diabetic treatment. It so happened that death came early from some
embolic or other accident, but the case nevertheless Ulustrates the benefit of
proper treatment of diabetes even in the presence of complicating conditions.

CASE NO. 26.

Female, age 14 yrs. American; schoolgirl. Admitted Dec. 7, 1914.

Family History. — No diabetes in family. Mother's mother died of cancer,
and mother's grandmother of "dropsy." Several more remote relatives died of
tuberculosis. Patient's father is healthy, the mother nervous but fairly strong.
There have been no other children and no miscarriages.

Fast History. — Girl has been healthy though rather nervous. Measles at 3,
chicken-pox at 4, mild whooping-cough at 5. She began school at 6th year, was
bright and studious but not overworked. Ate large quantities of candy. Al-
ways constipated. Fairly normal menstruation began at 12. For about 2 years
before the present illness there was frequent twitching of face, limbs, and trunk
during sleep. No such movements when awake.

Present Illness. — In Feb., 1913, the patient had an attack of vomiting after
eating heavily, and for a few days was nervous and without appetite. During
the following 3 weeks polyphagia, polydipsia, and polyuria were noted, also
weariness and sleepiness. Strength then failed progressively until she became
too weak to dress herself. A physician consulted in Mar. diagnosed diabetes and
prescribed carbohydrate-free diet. On this the patient remained sugar-free until
June, but lost weight even though bread and potatoes were gradually added to
diet. Glycosuria then reappeared, but remained absent from June to Dec. on
carbohydrate-free diet. It then became persistent, and a trip was made to
consult a specialist, who placed the patient in a hospital for 2 weeks and allowed
only small quantities of carbohydrate-free food. Glycosuria ceased but keto-
nuria persisted, and all symptoms recurred promptly on returning home. The
family physician then allowed an abundance of carbohydrate. The subsequent
symptoms have been the usual loss of weight and strength, and falling out of much
of the hair. Menstruation ceased with the first period after the onset of diabetes.

CASE RECORDS 281

Physkal Examination. — A tall, emaciated, nervous appearing girl, without
acute distress. Teeth in good condition. Tonsils not enlarged. No lymph
node enlargements. Skin dry. General physical examination negative. Right
knee jerk present, left not obtained. Achilles jerks lively. Blood pressure 105
systolic, 70 diastolic.

Treatment. — ^The glycosuria for 16 hours following admission was 44.5 gm.
On Dec. 8 to 10, under an observation diet of 30 to 65 gm. protein, 3 to 10 gm.
carbohydrate, and 900 to 1300 calories, the urine contained 6.8 to 14.3 gm. sugar
and showed heavy ferric chloride reactions. Fasting was begun Dec. 11, with
200 calories of alcohol daily. Glycosuria was absent in 24 hours. 140 gm. thrice
cooked vegetables were allowed on Dec. 13, 5 gm. carbohydrate in the form of
green vegetables on Dec. 14, and 9 gm. carbohydrate on Dec. 15. A trace of
glycosuria appeared. Nevertheless the vegetables were increased, up to 44 gm.
carbohydrate on Dec. 17, then diminished while two or three eggs were added.
With this continuance of undernutrition the trace of sugar cleared up. On Dec.
26 a diet of 51 gm. protein, 9 gm. fat, and 1200 calories caused another trace of
glycosuria, which cleared up with the fast-day of Dec. 27. Alcohol was discon-
tinued on Jan. 9. It was still given on fast-days to the extent of 200 calories,
up to Feb. 21. In early Jan., diets of approximately 40 gm. protein, 6 gm. car-
bohydrate, and 1000 calories twice caused slight glycosuria, which later cleared
up, and at the end of the month a diet as high as -80 gm. protein, 16 gm.
carbohydrate, and 1700 calories was borne without glycosuria. An attempt
on Jan. 30 and 31 to raise the carbohydrate to 25 gm. resulted in gly-
cosuria, checked by the routine fast-day of Feb. 1. In the succeeding week the
diet was further increased until on Feb. 5 to 6 glycosuria resulted from 90 gm.
protein, 30 to 40 gm. carbohydrate, and 2400 calories. Thereafter still higher
diets were tolerated, but on Feb. 27 glycosuria was produced by 84 gm. pro-
tein, 50 gm. carbohydrate, and 3000 calories. Not only the laboratory findings
but also the weakness and nervousness which were the essential complaints were
improved. Also, on admission there had been a marked albuminuria with
casts, but albumin gradually diminished to a trace and casts were absent. The
patient was discharged on Mar. 6, 1915, on a diet of 25 gm. carbohydrate, 75
to 80 gm. protein (2.5 gm. per kg.), and 2400 calories (almost 80 per kg.). The
regular weekly fast-days reduced the average to approximately 64 gm. protein
and 2100 calories. The prescribed diet was thus below what she had proved
able to tolerate.

Acidosis. — This was at no time threatening. The ferric chloride reaction
diminished as usual and became negative with the low diets of mid- January.
It will then be noted that increase of the total diet brought back well marked
ferric chloride reactions, even though carbohydrate was decidedly increased at
the same time.

Body Weight. — ^This was 31.2 kg. at admission. The undernutrition treat-
ment brought it down to its lowest point of 27.2 kg. on Jan. 26. Thereafter the

282 CHAPTER rn

higher diets produced a rise in weight, so that at discharge it was 30.7 kg.; i.e.,
0.5 kg. less than at admission.

Subsequent History.— The diet was faithfully followed. A few traces of glyco-
suria required a slight diminution of the carbohydrate allowance. On one occa-
sion a trace of glycosuria followed excitement due to having seen a woman run
over by a street car. The physical and psychic conditions remained good and
the patient enjoyed hfe and kept herself interested in various occupations not
involving exertion. Nevertheless, she tended to lose slightly in weight instead of
gaining. Menstruation did not return, but none of the former symptoms of
diabetes was present.

Second Admission. — Oct. 4, 1915, the patient returned to the hospital by
arrangement, for purposes of observation and for testing the effect of exercise.
Height 156.2 cm. Weight 28.8 kg.

The urine was stiU sugar-free, but showed a trace of ferric chloride which
disappeared with a single fast-day on Oct. 5. A tolerance test was then be-
gun in routine manner with 10 gm. carbohydrate in the form of green vege-
tables on Oct. 6. A trace of glycosuria appeared with 130 gm. carbohydrate on
Oct. 19, and persisted with the same intake the next day and with increased in-
take on the following days, notwithstanding the introduction of exercise at this
point in the attempt to raise tolerance. After the clearing up of glycosuria by a
sharp reduction of food on Oct. 24 to 25, a diet was gradually buUt up, with the
usual weekly fast-days. In the week of Nov. 22, a ration of 55 gm. protein, 15
gm. carbohydrate, and 2200 calories was tolerated without glycosuria, but with
ketonuria. With the same protein and carbohydrate, an increase of fat to 2400
calories in the following week brought on well marked continuous glycosuria,
and the damage thus done resulted in a continuance of glycosuria and ketonuria,
notwithstanding a sharp reduction of diet in the succeeding week (Dec. 6 to 11).
Low nutrition beginning Dec. 12 was continued throughout the remainder of the
stay in hospital. From Dec. 15 to Jan. 22, the protein was kept at 60 gm. daily.
The calories at first were 1200, but beginning Jan. 3 were diminished to 850.
Though all carbohydrate was omitted at the same time, this diminution in total
calories brought a complete clearing up of the ferric chloride reaction. Begin-
ning Jan. 24 another carbohydrate tolerance test was made. The assimilation
was found to be 140 gm., a gain of 20 gm. over the previous test. The patient
was discharged Feb. 26 on a diet of 30 gm. carbohydrate, 60 gm. protein (2.26
gm. per kg.), and 1000 calories (nearly 36 calories per kg.). This was reduced
one-seventh as usual by the regular fast-days, making the average daily intake
approximately 1.9 gm. protein and 33 calories per kg.

Acidosis. — The most striking feature is that well marked ferric chloride reac-
tions were produced by high calory diets in every instance, irrespective of whether
these diets contained carbohydrate. On lower diets suited to the patient's actual
tolerance there has been no difficulty in keeping this test continuously negative.
The ammonia excretion is also kept at a low level. The carbon dioxide capacity

CASE RECORDS 283

of the plasma tended to remain near or below the lower normal limit, but was
within normal limits at the time of discharge.

Blood Sugar. — Though this must have been high with the glycosuria resulting
from the carbohydrate test of Oct., yet, as usual when hyperglycemia is pro-
duced only by carbohydrate, it fell quickly, for on Oct. 25, after 2 days of low
diet, it was down to 0.13 per cent. It promptly rose to 0.26 per cent in the
plasma on the next day with continuance of a diet of 1200 calories and 15 gm.
carbohydrate. On the morning of Nov. 1, following the fast-day of Oct. 31, it
was down to the former approximately normal level. The curve ran similarly
through Nov., with hs^perglycemia on feeding and lower values following fast-
days, but with a general upward tendency. The diet up to 2400 calories, ending
Dec. 4, had produced such injury that the reduction to 1500 calories did not
prevent the occurrence of the highest blood sugars of the series; e.g., 0.32 on
Dec. 9 and 0.29 on Dec. 11, with glycosuria. This was one of the reasons for the
ensumg sharp reduction of diet. After 2 days of fasting on Dec. 12 and 13, the
sugar in the plasma on the morning of Dec. 14 was down to 0.155 per cent, and
in the whole blood down to 0.125 per cent. Thereafter the curve ran nearly
within normal limits, except for the sharp terminal rise on Feb. 25 to 0.224 per
cent. This occurred on 40 gm. carbohydrate, and the patient was sent home
with only 30 gm. carbohydrate in the diet. .

Body Weight. — At the second admission this was 2 kg. less than at the pre-
vious discharge, and at the second discharge it had been brought down still
lower. The net result of treatment from the first admission to the second dis-
charge was a reduction of weight by 4.9 kg. At home the patient's weight has
been constantly reported as approximately 60 pounds; i.e., about 27 kg., or 4
kg. less than at her first admission. There has been no appreciable growth in
height, but the patient was already almost as tall as her mother. She is notice-
ably emaciated, but the graphic chart well illustrates that every gain of weight
brought on glycosuria and acidosis. In order to Uve, the patient must keep her
weight down. It is not only inadvisable but impossible to force the weight up,
for any diet exceeding her tolerance as respects food and weight wiU quickly
bring on active diabetic symptoms, which of themselves would lead to loss of
weight.

Exercise. — The second period in hospital was devoted largely to a clinical test
of exercise in this patient. During the carbohydrate tolerance test in Oct. she
was kept at rest until the first trace of glycosuria appeared. She was then ex-
ercised to the limit of her strength, chiefly by climbing stairs and walking, also
by roller-skating and tossing the medicine ball. The glycosuria did not cease,
and no gain in tolerance could be demonstrated. Subsequently high diets were
given, as stated, from the latter part of Oct. to the forepart of Dec; and the
patient, who was moderately strong, was exercised regularly to her utmost ca-
pacity in the attempt to bum off the surplus calories. The low plasma bicarbon-
ate during this time is doubtless due in part to exercise. It proved impossible to

284 CHAPTER in

prevent hyperglycemia and finally glycosuria by this means, and the ferric
chloride reaction became positive when exercise was thus taken to bum up the
fat, though on lower fat intake it was negative even without exercise. Accord-
ingly in Dec. the diet was reduced as above mentioned. Exercise was still
continued.

From Dec. 12, 1915, to Jan. 23, 1916, three influences were present, namely,
carbohydrate abstinence, undernutrition, and hard muscular exercise. Never-
theless, the absence of any noteworthy acidosis is demonstrated by all tests.
The rise of 20 gm. in tolerance shown by the carbohydrate test in Feb. is merely
what might be expected from the undernutrition treatment, and there is no
indication that the 4 months of hard systematic exercise had served specifically to
increase tolerance.

Subsequent History. — ^At the time of discharge the patient was advised to dis-
continue severe exercise and take only as much as she could enjoy. She has
foimd pleasure in spending much of her time in walking, bicycling, and various
forms of active play. What has actually been accomplished by exercise is a
decided gain in strength, general health, and happiness. The change, as com-
pared with the first admission when she was kept nearly at rest, is evident at a
glance, and friends complimented her on her improved color and appearance.
Nervousness and worry are also controlled, and she is enabled to derive some real
enjoyment from life.

Glycosuria has remained absent except for rare traces due to unintentional
excesses; e.g., traces resulted from the use of cream cheese or sugar cured ham.
By June 19 she had lost three quarters of a poxmd in weight, but this was slightly
more than regained by Sept. In the fall she undertook light school work. In
Nov. and Dec. she had two colds and showed traces of sugar several times in
consequence, so that carbohydrate had to be entirely eliminated from the diet on
some occasions. In Apr., 1917, the patient reported having finished the first year
of high school and having easily obtained the highest mark in every subject.
Her diet has been modified to consist of 40 gm. protein, 10 gm. carbohydrate, and
1000 calories. She keeps herself sugar-free without difficulty and knows how to
treat herself if accidental causes bring on traces of glycosuria.

Remarks. — This patient, when received, presented a case of juvenile diabetes
of 2 years standing and considerable severity. The subsequent treatment illus-
trates especially two points. One is the effect of exercise. The case was of
such severity that the deficiency of the pancreas could not be balanced to any
appreciable extent by improved function and activity of the muscles. Accordingly
the carbohydrate tolerance was not perceptibly improved, but the general health
was greatly benefited. Second is the question of growth and nutrition. Here
the clinical experiment was performed of taking this patient, clearing up her
condition radically by undernutrition, so that about the middle of Jan., 1915,
she was entirely free from both glycosuria and acidosis, and then making the
attempt to have her grow and develop. The diets in the latter half of the first

CASE RECORDS 285

hospital period were plarmed to this end. The weight rose, but symptoms shnul-
taneously returned. The diet at this discharge represented approximately 2.25
gm. protein and 80 calories per kg. of body weight. Fasting and modifications of
diet required by the occasional traces of glycosuria absolutely prevented gain or
growth. It is not known whether a specific diabetic deficiency also may be con-
cerned. The net result of this attempt to put on weight was, as stated, that the
patient returned to the hospital 7 months later, weighing 2 kg. less than at
discharge.

After the undernutrition represented by the Oct. carbohydrate test, the diet
was gradually built up, the weight rose with it, and the maximum of weight and
the onset of urinary symptoms coincided (Dec, 1915). Subsequently undernu-
trition diminished the weight and removed all active symptoms. It is obvious
throughout that the total diet was the essential governing factor, and the relative
proportions of protein, carbohydrate, and fat were of minor influence. The net
result to date is that the patient is alive 3 years from the beginning of this treat-
ment, and 4| years from the onset of her diabetes. There is no evidence of any
spontaneous downward progress; neither has there been any fundamental'im-
provement. The cumulative effect of slight strains and accidents may bring
bad results sooner or later. Meantime, the patient is holding her own and is
actually deriving enjoyment from Kfe and carrying on limited activities. The one
requisite is close- control of her diet.*

CASE NO. 27.

Male, married, age 42 yrs. American; clerk. Admitted Jan. IS, 1915.

Family History. — One sister died of cardiorenal disease at 23. Family his-
tory otherwise negative. Patient has been married 18 years and has one healthy
son, aged 15. Wife healthy; one miscarriage about 13 years ago.

Past History. — Healthy life. Good hygienic surroundings. Measles and
chicken-pox in childhood; mild diphtheria at 8; mumps at 18, complicated by
unilateral orchitis. At about 20 there was an attack of jaundice with clay-
colored stools lasting 2 or 3 days. At 26 one attack like acute appendicitis,
which passed off under ice applications in a hospital. There have been indefi-
nite minor attacks since. At 27 patient had fever every night for 28 days, with
one hard chill at the end; then given medicine by family physician and has had
nothing like malaria since. Occasional sore throats; never tonsillitis. Vene-
real disease or exposure denied. Habits regular; no excesses in alcohol, tobacco,
or food. .

* Word has been received of the patient's death in Feb., 1918. The child her-
self was faithful and contented, but the parents concluded to try an independent
experiment to "build her up." The child was kept in ignorance of the glycosuria
which quickly followed the increased diet, and the fatal outcome was due solely
to this foUy of the parents.

286 CHAPTER III

Present Illness. — 8 years ago patient began to feel rather poorly, also had
serious trouble with his teeth. Numerous teeth had to be extracted, and he de-
veloped an infection of the mandible, some of which sloughed away. His physi-
cian diagnosed diabetes. The carbohydrate in his diet was diminished but
other foods were not restricted. Since that time he has had occasional attacks of
polydipsia, otherwise no diabetic symptoms, except more or less continuous trouble
with his teeth. Some recent worries apparently made the condition worse, but
he remained in fair health and able to work until Jan. 3, 1915, when his neck
began to pain and swell. He was immediately taken in charge by an eminent
New York surgeon who had been an old-time friend. The pain required mor-
phine, and the fever and progressive advance of the border of infection were so
threatening that the surgeon contemplated complete excision of the infected
area and brought the patient to this Institute with the intention of operating the
same or the following day.

Physical Examination.— Height 169 cm. Weight 59.6 kg. A well developed,
fairly well nourished man, with fever, flushed face, unduly bright eyes, and ap-
pearance of prostration. Numerous teeth missing; much caries and pyorrhea.
On the left side of the neck behind, there is a very large carbuncle with its
apex about midway between the postaural line and the posterior median line,
and with marked redness and induration extending past the posterior median
line behind and to the internal border of the sternocleidomastoid in front. The
whole area is intensely tender and movements of the neck are prevented. Physi-
cal examination otherwise negative.

Treatment. — Fever was continuous, but the highest temperature was 102.5.°
Morphine was required to control pain, particularly at night. There was a
heavy ferric chloride reaction, and the urine on the 1st day contained 36.4 gm.
sugar, on the 2nd day 32.4 gm. The diet on this day Qan. 16) was 87 gm. pro-
tein, 11 gm. carbohydrate, and 1400 calories. The general condition was criti-
cal, and the surgeon felt impelled to operate by the approach of the infection to
the plane of the great vessels of the neck; but in view of the acidosis and nega-
tive carbohydrate balance it was advised that operation be postponed for at least
a day or two until the influence of fasting could be brought to bear. Accordingly,
fasting was begun on Jan. 17, with as much whisky as could be comfortably
taken for the sake of keeping up strength. The quantity of alcohol thus taken
was from 700 down to 500 calories daily. After 1 day of fasting the glycosuria
had fallen to 9.75 gm. and the general condition was at least no worse. The
glycosuria continued to diminish on the following days and was absent on the
4th day of fasting. Meanwhile the general condition improved, pain dimin-
ished, the apex of the carbuncle began to discharge pus, and the night of Jan. 21
was the first on which morphine was not required. 2 days of complete freedom
from glycosuria were allowed to pass before the addition, on Jan. 22, of 9 gm.
carbohydrate in the form of tomatoes, celery, and lettuce to the daily allowance
of whisky. On Jan. 23 this was raised to approximately 20 gm., and on Jan.

■ CASE RECORDS 287

24 to 30 gm. On account of traces of glycosuria it was diminished on the follow-
ing days to 6 gm., and following that both whisky and carbohydrate were in-
creased, so that from Feb. 7 to 27 the diet was usually just below 40 gm. carbo-
hydrate and 100 gm. alcohol daily. The fever had gradually fallen, but the
temperature remained between 99° and 100°F. until Jan. 31, after which it was
normal. The core of the carbuncle was extruded on Jan. 30, but full healing of
the large local inflammation was not complete until Mar. 1. With continuance
of the diet mentioned, the traces of glycosuria became less frequent as the in-
fection cleared up, so that the allowance of 40 gm. carbohydrate and 100 gm.
alcohol was fully tolerated.

Beginning Mar. 1 a diet was gradually built up, at first containing only some
20 gm. protein and SOO non-alcohol calories, but rising by Apr. 8 to 115 gm. pro-
tein, 40 gm. carbohydrate, and 2650 calories. Whisky was then discontinued
and, except for the fast-day of Apr. 11, was not used again even on fast-days. A
regular diet was planned consisting of 90 to 100 gm. protein, 25 gm. carbohy-
drate, and 2000 to 2200 calories; this was in the neighborhood of 2 gm. protein
and 40 calories per kg. of body weight, reduced one-seventh by the weekly fast-
day, so that the actual average was nearly 1.5 gm. protein and 35 calories per kg.

After the initial critical infection was overcome, the patient had been left weak
and debilitated, complaining of pains in the legs and other parts of the body.
The blood pressure on Feb. 11 was down to 90 systolic, 70 diastolic. He gained
strength while losing weight, and still more as his weight was slightly built up.
He was encouraged to begin exercise as soon as strength permitted, and this
was increased until at the time of discharge he was taking long walks daily. He
had not only regained the condition present before the carbuncle, but had reached
a state of health better than at any time during the previous years of diabetes.
He was discharged to undertake his regular work.

Acidosis. — ^This was measured at the outset only by the ammonia excretion,
which was modified by alkali dosage. As a measure of precaution against the
acidosis to be feared with an infection, sodium bicarbonate was given beginning
Jan. 16. On this day the total taken was 15 gm., on the next day 40 gm., and
this daily quantity was continued with scarcely any change until Feb. 3, when it
was diminished to 10 gm. On Feb. 7 it was increased to 20 gm., on Feb. 10 to
30 gm., and on Feb. 19 to 40 gm. This was continued until Feb. 23, when it
was abruptly stopped. On Mar. 3, 10 gm. soda were begun and continued to
Mar. 13, after which soda was permanently discontinued.

The chart gives the impression that the patient had been threatened with a
serious acidosis. The low ammonia value shown on the day of admission repre-
sents only part of a day. The excretion of approximately 1.4 to 1.6 gm. ammonia
nitrogen Jan. 17 to 21 occurred in spite of the considerable alkali dosage men-
tioned. The carbon dioxide capacity of the plasma was kept within normal
limits during this alkali treatment, at least after Jan. 29. High normal values
were present on Feb. 18 to 22 with 30 to 40 gm. bicarbonate daily, and the am-

288 CHAPTER III .

monia nitrogen was also down to the low figure of 0.25 to 0.35 gm. Promptly
with the omission of soda on Feb. 23 the plasma bicarbonate fell sharply and the
ammonia began a corresponding steep rise. On Mar. 2 the CO2 capacity touched
its lowest point of 43 .6 vol. per cent, and the ammonia N on the same day had risen
to 2.8 gm. The use of 10 gm. sodium bicarbonate daily, beginning Mar. 3, pro-
duced a rather prompt rise of the plasma bicarbonate. The ammonia fell only
shghtly, then rose to an actually higher level on Mar. 8. The increase of pro-
tein in the diet was presumably one factor. By Mar. 13, however, the ammonia
nitrogen was down to 1 .68 gm. By this time the strength of the acidosis seems to
have been broken. On Mar. 24, without alkali, the ammonia was slightly lower
(1.4 gm. N). The next day it fell sharply to 0.56 gm., and almost simultaneously
the ferric chloride reactions became light for the first time. The ammonia was
equally low on the fast-day of Apr. 4. With the high diets of Apr. 5, 6, and 7
it was higher, and fell again on the fast-day of Apr. 11. After that it varied
between 0.4 and 1.25 gm. N. Likewise, following the discontinuance of alkali
on Mar. 13, the plasma CO2 capacity remained little changed until Mar. 19^
The tests on Mar. 24 and 30 showed it falling rapidly, but it stopped at 44.2 per
cent, and then rose spontaneously within normal limits without the aid of alkali.

The impression is given that alkali was a useful temporary aid in this case.
The milder grades of acidosis may be ignored, and the severer ones also can fre-
quently be treated successfully without alkaU, but when there is a tendency to
serious acidosis overtaxing the defenses of the alkaUne reserve of the body, both
comfort and safety are apparently served by the use of sufficient quantities of
alkali, which are discontinued when proper treatment has overcome the essential
condition imderlying the acidosis.

The ferric chloride reaction was heavy at admission and became intense fol-
lowing the use of soda. It proved very persistent, in conformity with the other
manifestations of the tendency to acidosis. The condition being satisfactory in
other respects, this reaction was left to wear itself out with time and improve-
ment of tolerance. As stated, it became negative some months after discharge,
and has not reappeared.

Blood Sugar. — Analyses were made during the latter part of the hospital period,
and the relatively low values found constituted one feature of the favorable
picture.

Weight and Nutrition. — ^The steep fall in weight, which was intentionally re-
duced from 59.6 kg. on Jan. 16 to 47 kg. on Mar. 4 — a loss of 12.6 kg. in 48 days —
is one of the noticeable features of the treatment. It was necessary first to con-
•trol radically the diabetes which was responsible for the susceptibility to infec-
tion. Second, it was necessary to build up tolerance for carbohydrate and other
foods, in order to save the patient from the persistent acidosis and weakness.
These objects were accomplished by rigorous undernutrition. The patient with
acute infection and fever was subjected to 5 days of fasting with alcohol. After
that, nothing but a little green vegetables was added up to Mar. 1, the idea being

CASE RECORDS 289

to continue undernutrition while combating acidosis by the use of carbohydrate
to the limit of tolerance under the conditions of highest tolerance; viz., exclusion
of other food. Except for these green vegetables, there was complete depriva-
tion of solid food for the 42 days from Jan. 17 to Mar. 1. The fall in weight
was therefore to be expected, and from the urea and ammonia curves it is also
possible to estimate a considerable loss of body nitrogen. It is to be empha-
sized that under these conditions the resistance to infection apparently, and the
general strength certainly, irnproved. Weakness and lowered resistance are to
be regarded as due more to the specific diabetic disorder than to depletion of
food materials, and the policy of trying to strengthen diabetic patients by feeding
in excess of the tolerance is an injurious one.

After the crisis was past, the condition gradually began to assume its proper
proportions as a comparatively mild case of diabetes. In view of the patient's
age and the demonstrated food tolerance, a fairly liberal diet was built up,
sufficient for health and efficient work, and a moderate gain of weight was also
permitted. At discharge, however, the weight was only 50.4 kg.; i.e., 9.2 kg.
below the weight at entrance. The patient has since obeyed the injunction not
to put on much flesh, and is now thin, wiry, and strong.

Subsequent History. — The patient adhered to his diet and remained free from
glycosuria except for a trace on June 18, after ISO gm. strawberries for break-
fast. A moderate ferric chloride reaction was still present on Dec. 27, 1915,
but cleared up not long after that. He later undertook work which made diffi-
cult the accurate weighing of food, and he was therefore allowed to estimate the
quantities from his previous experience. He has since remained free from glyco-
suria, ketonuria, and all symptoms. He feels as well as at any time in his life
and has risen to the position of cashier.

The carbuncle made the diabetes worse, but the mouth condition was seemirigly
the result rather than the cause of the diabetes; for after the therapeutic con-
trol of the diabetes, the patient now with ordinary dental care remains free from
tooth trouble.

Remarks. — ^This was one of the difficult cases of serious infection which may
cause even mild diabetes to turn suddenly severe, incidentally illustrating the
functional as opposed to the organic element in human diabetes. Numerous
fatalities are inevitable with such a combination. The favorable outcome in this
case must undoubtedly be attributed largely to the fact that the carbuncle was
near the point of discharging spontaneously, so that a few days of fasting are
not to be credited with radical cure of the infection. On the other hand, good
evidence is afforded that the resistance was not lowered by fasting, and the be-
lief is that it was raised. Likewise the subsequent treatment by undernutrition
has not made the patient susceptible to infections and other mishaps, but has
on the contrary relieved him of these and all other diabetic complications.

290 CHAPTER III

CASE NO. 28.

Female, age 11 yrs. American; schoolgirl. Admitted Jan. 19, 1915.

Family History.— A paternal granduncle died of tuberculosis some years ago.
No other disease in family. Father, mother, and one brother of patient entirely
weU.

Past History.— Healthy life. Whooping-cough at 5, measles at 6, and mumps
at 10. A strong, active child, Uving imder good hygienic conditions in a small
town in New York. In Aug., 1913, she had fever for 24 hours. Temperature
was as high as 104°, and the physician could make no diagnosis. There were a
few cases of poliomyelitis in the neighborhood about that time. For a short
time afterward, the patient was subject to nervous movements and had pain
in ankles without objective signs of inflammation. Habits always regular. Dis-
position not nervous. She has been on the honor roll at school, but has been
kept from overstudy.

Present Illness. — While visiting in New York City after New Years day this
year, polyuria was noticed, and when this continued several days the patient's
mother suspected diabetes, and the diagnosis was made by her physician. The
nervous movements noted after the previous illness were now increased. A diet
was prescribed excluding most ordinary carbohydrates, but including gluten bread,
toast, and milk.

Physical Examination. — A healthy looking girl, well nourished and rather
large for her age. The face appears nervous, and there are twitching or chorei-
form movements of the head and arms. Teeth in good condition. Tonsils
hypertrophied. Enlargement of epitrochlears but not of other lymph nodes.
Knee and other reflexes exaggerated. Examination otherwise negative.

Treatment.^-The glycosuria of 1.6S per cent present when patient was brought
to the hospital ceased immediately on a carbohydrate-free diet of 600 to 650
calories, but the ferric chloride reaction, which had been negative, developed in
moderate intensity on the second day of this diet. 2 fast-days were then im-
posed Qan. 21 and 22), and the ferric chloride color became intense. Green
vegetables were begun in the usual manner on Jan. 23 and increased until the
limit of tolerance seemed to be reached with 133 gm. carbohydrate on Feb. 1.
Instead of a fast-day on Feb. 2, the vegetables were merely diminished to 36
gm. carbohydrate. Under this program the ferric chloride reaction had become
much paler, the ammonia nitrogen had fallen from 0.85 gm. on Jan. 25 to very
low figures, and the plasma bicarbonate had risen from 47 per cent on Jan. 25
up to the lower normal Umit. Carbohydrate-free diet was begun on Feb. 3 with
two eggs, 20 gm. butter, and 250 gm. thrice cooked vegetables. This diet was
rapidly increased and carbohydrate introduced. On Mar. 1 to 3 the patient
proved able to tolerate 80 to 90 gm. protein, 50 gm. carbohydrate, and 3000
calories, without glycosuria but with persistence of a sUght ferric chloride reac-
tion. She was discharged Mar. 5 on a diet of 72 gm. protein, 30 gm. carbohy-
drate, and 2500 calories (approximately 2.5 gm. protein and 90 calories per kg.).

292 CHAPTER m

lation was actually diminished. Carbohydrate up to 140 gm. was tolerated per-
fectly, then heavy glycosuria occurred. The child was brought to confess that
this was due to stealing bread, and that the difficulties in the preceding months
had been due to the same cause. By Oct. 12 she was taking 75 gm. protem,
30 gm. carbohydrate, and 1500 calories, weighed 86 pounds, and had grown 2i
inches since leaving hospital. On Jan. 10, 1917, the first menstrual period ap-
peared in normal manner, but none has appeared since that time. The re-
port on Jan. 18, 1917, showed that she was taking 80 gm. protein, 24 gm. carbo-
hydrate, and 1625 calories, and weighed 901 pounds.

In Mar., 1917, she went through German measles without glycosuria. There
have been occasional traces of glycosuria, the trouble being partly due to indulgent
management, but these traces are always cleared up immediately and com-
pletely by fasting. The patient feels and appears entirely well and is continuing
normal activities.

Remarks. — The history suggests that this is a case of diabetes resulting from
an acute infection. If so, the damage produced was not transitory. The pa-
tient remains diabetic, and is liable to take an unfavorable turn from some acci-
dental disturbance at almost any time; spontaneous downward progress is not
noted. There is a definite improvement, but not to any extent suggesting a
complete cure. If such improvement can continue the ultimate outcome may be
very favorable. Actual recuperation to this degree, especially on rather high
diets, is unusual, and possibly stands in relation to an exceptional etiology. If
diabetes is caused by a transitory infection, the repair of the damage may some-
times be partial instead of complete. Possibly childhood may actually favor re-
pair under the special conditions. In the absence of complete recovery, there is
no doubt that neglect of diet will entail rapid downward progress. Dietetic
treatment may save in proportion as it is early and effective. If the improve-
ment can continue, the ultimate outcome in this particular patient may be very
favorable. Thus far at any rate, in this case of juvenile diabetes, taken at an
early, fairly mUd stage, it has been possible through 2 J years to obtain improve-
ment rather than downward progress, along with seemingly normal growth and
development.*

CASE NO. 29.

Female, unmarried, age 26 yrs. Finnish; domestic. Admitted Jan. 27, 1915.

Family History. — ^Parents are living; both have heart trouble. One brother is
well. Two sisters died of tuberculosis and three others of unknown causes in
adult life. Family history otherwise negative for tuberculosis, cancer, syphilis,
and diabetes.

Past History. — Healthy life, spent in comfortable circumstances on farm in
Finland up to 3 years ago, since then patient has been employed as domestic

* A relapse has occurred, and the patient has been referred elsewhere for treat-
ment. The experience is a further warning of the pernicious effect of high diets.

CASE RECORDS 293

in the better parts of New York. For the past i months she has been a cook.
No illness remembered, except whooping-cough in childhood. Occasionally-
patient spits a little bright red blood. Diet has been rich in starch but not in
sweets. No excesses or bad .habits.

Present Illness. — ^Just after the recent Christmas holidays the patient first
noticed weakness, weariness, polyphagia, polydipsia, and the loss of IS pounds
weight. A physician immediately diagnosed diabetes.

Physical Examination. — A well appearing, fairly well nourished young woman.
Teeth in good condition. Throat sUghtly congested; tonsils show neither hy-
pertrophy nor exudate. Cervical, epitrochlear, and inguinal lymph nodes not
palpable. Axillary glands are shot-like. General examination negative. Blood
pressure 110-90.

Treatment. — ^The partial urine specimen on the day of admission showed 1.69
per cent, or 7.52 gm. sugar. On the next day (Jan. 28), on a carbohydrate-free
observation diet of 68 gm. protein and 1350 calories there was glycosuria of only
2.1 gm. Anorexia had come on before admission, so this diet was aU the patient
cared to take. On Jan. 29 fasting was begiin^ and on the subsequent days as
much as 100 cc. whisky were allowed; larger quantities could not be taken be-
cause of nausea. The urine immediately became sugar-free, but a weU marked
ferric chloride reaction persisted, partly perhaps because of the use of sodium
bicarbonate. Because of the slightly subnormal CO2 capacity of the plasma
and the seeming tendency to weakness and nausea, 50 gm. sodium bicarbonate
had been given on the first day of fasting (Jan. 29) and 100 gm. on the second
fast-day (Jan. 30). The cUnical condition was not perceptibly altered, and
gave no indication of either benefit or injury. On Jan. 31, after the urine had
been sugar-free over 72 hours, green vegetables were allowed containing 5 gm.
carbohydrate. This quantity was increased up to 100 gm. carbohydrate on
Feb. 4 and 5. This was tolerated without glycosuria. But with the protein-fat
diet of 1200 to 1700 calories (Feb. 8 to 12), traces of glycosuria occurred
with an intake of only 9 gm. carbohydrate.

Owing to the persistence of ferric chloride reactions, another period of alcohol
and green vegetables was given up to Feb. 25. Thereafter only traces of glyco-
suria resulted from very high diets; e.g., 90 gm. protein, 35 gm. carbohydrate,
and 3600 calories on Mar. 8 to 10. The diet was then adjusted so that at dis-
charge on Apr. 21 it consisted of 90 gm. protein, 50 gm. carbohydrate, and nearly
3000 calories (approximately 2 gm. protein and 70 calories per kg.). The weight,
which had been markedly reduced during undernutrition up to Feb. 25, increased
on the higher diets, so that at discharge it was almost at the admission level.

All symptoms had disappeared and the patient felt entirely well. Radio-
graphs and repeated sputum examinations failed to reveal any tuberculosis.

In Apr. the patient received word that her only brother had died of tubercu-
losis. She therefore insisted upon returning to Finland. The bad news and the
preparations for departure brought on no glycosuria. She was given a letter to
a professor in Helsingfors, and was warned to remain free from glycosuria under
all conditions.

294 CHAPTER ni

Remarks. — ^The case is not instructive. Even with allowance for the weekly
fast-days the diet was too high for permanently good results. The patient was
ignorant of the gravity of her condition and it was judged that she would not ad-
here to any serious restrictions, and this became more certain when she decided
to return to Finland. Rather than have her break away from restrictions alto-
gether, it seemed advisable to plan a diet adequate to permit her to work and
feel well for the present and not attempt a more ideal result. Nothing has been
heard of the patient since discharge.

CASE NO. 30.

Female, married, age 45 yrs. American; housewife. Admitted Jan. 30,
1915.

Family History.— FsLthei is living, aged 72. Mother died at 47, following
operation for fibroids. One sister died at 35, following operation for an old
traumatic hip; three sisters are well. No diabetes or other special diseases
known in family. Patient has been married 25 years and has had seven chil-
dren; three are alive and well, the others died in infancy when the mother was in
bad condition or suffering from grippe or typhoid.

Past History. — Usual childhood diseases (history indefinite). Typhoid fever
25 years ago. Grippe at several times; no sore throat. Appendicitis 8 years ago;
operation. 7 years ago curettage for menorrhagia. Operation for mastoiditis 6
years ago. For some years past the patient has been nervous and suffered from
nervous indigestion. Feces have also been pale, but never showed blood. Habits
have been regular, diet simple; no excesses.

Present Illness. — First symptom was pruritus vulvae 7 months before admission,
followed by marked polyphagia, polydipsia, and poljTiria. She sought no treat-
ment for 4 months, then was placed on a diet, carbohydrate-free except for green
vegetables and one sUce of toast. She has lost 35 pounds weight. During 2
days prior to admission to hospital her physician had placed her on absolute
fasting with whisky and sodium bicarbonate.

Physical Examination. — ^Woman without dyspnea or acute symptoms, moder-
ately weak. Body shows evidence of considerable loss of weight, but still carries
fair quantity of fat. Eyes react normally and ophthalmoscopic examination is
negative. Teeth are in good repair. Throat congested; tonsils free from exu-
date or hypertrophy. Cervical and inguinal glands not palpable, axillaries and
epitrochlears slightly enlarged. Knee jerks obtained only on reinforcement, and
then sluggishly. Achilles jerks present. Blood pressure 110 systolic, 85 diastolic.
General examination negative.

Treatment. — Patient seemed in fair condition and in no danger when admitted.
Only shght glycosuria was present, and only a moderate ferric chloride reaction.
She was admitted in the afternoon and received supper consisting of soup, 100 gm.
steak, and 100 gm. raw and 100 gm. thrice cooked vegetables. She was men-
struating, and had slight diarrhea. A phenolphthalein tablet and 15 gm. mag-

CASE RECORDS 295

nesium sulfate produced small liquid or soft movements which continued undSr
small doses of cascara on the following days. On the first full day in hospital
(Jan. 31) the diet consisted of 81 gm. protein, 5 gm. carbohydrate, and 1650 cal-
ories. Glycosuria was entirely absent, the ferric chloride reaction still only
moderate, and the condition apparently satisfactory. The next day, Feb. 1,
the diet consisted of SO gm. protein, 12 gm. carbohydrate, and 1250 calories. The
patient showed slight nausea. On Feb. 2, the diet consisted of coffee, soup, one
egg, and 600 cc. milk, representing 27 gm. protein, 30 gm. carbohydrate, and 500
calories. Nausea had increased, and on this day the patient vomited once a
little undigested food. She said she had often had such attacks with her indi-
gestion in the past. With small doses of chloretoUe, also a Seidlitz powder fol-
lowed by a saline enema which removed considerable feces, the nausea seemed
greatly diminished. Meanwhile a trace of glycosuria had appeared from the
carbohydrate, and the ferric chloride reaction had become intense, but the highest
ammonia nitrogen output (Feb. 2) was 1.9 gm. On Feb. 3, the diet was limited
to 300 cc. clear soup, 300 cc. milk, and 90 cc. whisky. The patient also received
3 cc. aromatic cascara, 30 cc. Pluto water, and 10 gm. sodium bicarbonate. On
Feb. 4, as glycosuria and ketonuria were well marked and the patient was slightly
nauseated, a fast-day was given, the entire intake being 150 cc. coffee, 130 cc.
whisky, 15 gm. sodium bicarbonate, 3 cc. aromatic cascara, and 30 cc. Pluto
water. Though the urine remained acid, the glycosuria diminished to a trace,
ammonia fell to 0.87 gm. N, and the CO2 capacity of the plasma, which had been
only 35.8 per cent on Feb. 2, rose to 57.7 vol. per cent on Feb. 4. Feb. 5 was also a
fast-day, the intake being 140 cc. whisky and 15 gm. sodium bicarbonate. The
urine remained acid. In the morning the patient felt well; toward evening she
was slightly dizzy and nauseated. Feb. 6 was also a fast-day with 125 cc. whisky
and 25 gm. sodium bicarbonate. The symptoms were more alarming; the tem-
perature was 99.2°F., the pulse 90, the respiration 20; the pulse was weak, and the
patient complained of dizziness and vomited several times. Two doses of 0.5
gm. chloretone were given for the vomiting, and 2 gm. compound jalap powder
to empty the bowels further, though there had been one or more defecations
every day.

On Feb. 7 only 25 cc. whisky could be taken because of nausea. Vomiting
continued notwithstanding the use of a variety of routine measures, and weakness
was becoming serious. The temperature first was as high as 99.8°, but fell by
the close of the day to 96°. The pulse ranged 100 to 130, the respiration 28 to
44. Caffeine was administered at intervals subcutaneously, and later camphorated
oil. An attempt also was made to feed, and milk, eggs, and beef juice were
given and partly vomited. 1 liter of 4 per cent sodium bicarbonate solution was
successfully given by the rectal drip method. The patient had become very
drowsy, almost unconscious.

On Feb. 8, eggs and beef juice were continued, as also the caffeine and cam-
phorated oil. Levulose was also given in small doses totahng 140 gm.; it was

CASE RECORDS 295

nesium sulfate produced small liquid or soft movements which continued under
small doses of cascara on the following days. On the first full day in hospital
(Jan. 31) the diet consisted of 81 gm. protein, 5 gm. carbohydrate, and 1650 cal-
ories. Glycosuria was entirely absent, the ferric chloride reaction still only
moderate, and the condition apparently satisfactory. The next day, Feb. 1,
the diet consisted of SO gm. protein, 12 gm. carbohydrate, and 1250 calories. The
patient showed slight nausea. On Feb. 2, the diet consisted of coffee, soup, one
egg, and 600 cc. milk, representing 27 gm. protein, 30 gm. carbohydrate, and 500
calories. Nausea had increased, and on this day the patient vomited once a
little undigested food. She said she had often had such attacks with her indi-
gestion in the past. With small doses of chloretotxe, also a Seidlitz powder fol-
lowed by a saline enema which removed considerable feces, the nausea seemed
greatly diminished. Meanwhile a trace of glycosuria had appeared from the
carbohydrate, and the ferric chloride reaction had become intense, but the highest
ammonia nitrogen output (Feb. 2) was 1.9 gm. On Feb. 3, the diet was limited
to 300 cc. clear soup, 300 cc. milk, and 90 cc. whisky. The patient also received
3 cc. aromatic cascara, 30 cc. Pluto water, and 10 gm. sodium bicarbonate. On
Feb. 4, as glycosuria and ketonuria were well marked and the patient was slightly
nauseated, a fast-day was given, the entire intake being 150 cc. coffee, 130 cc.
whisky, 15 gm. sodium bicarbonate, 3 cc. aromatic cascara, and 30 cc. Pluto
water. Though the urine remained acid, the glycosuria diminished to a trace,
ammonia fell to 0.87 gm. N, and the CO2 capacity of the plasma, which had been
only 35.8 per cent on Feb. 2, rose to 57.7 vol. per cent on Feb. 4. Feb. S was also a
fast-day, the intake being 140 cc. whisky and 15 gm. sodium bicarbonate. The
urine remained acid. In the morning the patient felt well; toward evening she
was slightly dizzy and nauseated. Feb. 6 was also a fast-day with 125 cc. whisky
and 25 gm. sodium bicarbonate. The symptoms were more alarming; the tem-
perature was 99.2°F., the pulse 90, the respiration 20; the pulse was weak, and the
patient complained of dizziness and vomited several times. Two doses of 0.5
gm. chloretone were given for the vomiting, and 2 gm. compound jalap powder
to empty the bowels further, though there had been one or more defecations
every day.

On Feb. 7 only 25 cc. whisky could be taken because of nausea. Vomiting
continued notwithstanding the use of a variety of routine measures, and weakness
was becoming serious. The temperature first was as high as 99.8°, but fell by
the close of the day to 96°. The pulse ranged 100 to 130, the respiration 28 to
44. Caffeine was administered at intervals subcutaneously, and later camphorated
oil. An attempt also was made to feed, and milk, eggs, and beef juice were
given and partly vomited. 1 liter of 4 per cent sodium bicarbonate solution was
successfully given by the rectal drip method. The patient had become very
drowsy, almost unconscious.

On Feb. 8, eggs and beef juice were continued, as also the caffeine and cam-
phorated oU. Levulose was also given in small doses totaling 140 gm.; it was

296 CHAPTER m

retained but had no evident effect. At 4 p.m., 700 cc. 4 per cent sodium bicar-
bonate were given intravenously. At 10 p.m. 100 cc. were likewise given. The
temperature had slowly risen, and continued to rise, reaching 101° F. at 7 p.m.
on Feb. 8, 101.8° at 1 a.m. on Feb. 9, and 104° at 5 a.m. The pulse remained
about 140, the respiration 40 to 48. Toward the close the picture was that of
fully developed diabetic coma. Death occurred at 6:45 a.m. on Feb. 9.

Remarks. — ^This was the first case seen at this Institute showing development
of fatal acidosis on fasting, and the treatment was mistaken because the condi-
tion was unexpected. The very rapid loss of weight, from 56.8 kg. on Jan. 31,
down to 52.2 kg. on Feb. 7, is a significant feature apparently present in all such
cases. One error in treatment is the low fluid intake and correspondingly low
output as shown in the graphic chart. Salts should also have been more liberally
suppUed. But the chief lesson for such cases is to break off fasting when the
first warning symptoms appear, and after a period of some days of feeding to
repeat the fast, which then is well borne. Suitable preparatory feeding preceding
the initial fast will doubtless also prevent all or nearly all such mishaps.

CASE NO. 31.

Male, unmarried, age 35 yrs. American; real estate agent. Admitted Feb.
12, 1915.

Family History. — Mother is well except for occasional rheumatism. Father
died of sarcoma at 62. One brother and two sisters are well; two died in in-
fancy. No knowledge of any family disease.

Fast History. — Patient has lived all his life in New York City in good health
and hygienic surroundings. Measles and whooping-cough in childhood. Gonor-
rhea 10 years ago. SyphiUs denied; two Wassermann tests in the past have
been negative. In 1889, after ^exposure to a great blizzard in winter, the patient
suffered from inflammatory rheumatism in the spring. This returned almost
yearly until 1895, when he received treatment by medicine, which ended the
rheumatism permanently but left him with persistent bad digestion. 12 years
ago he had St. Vitus' dance, which was cured in a German sanitariimi b}'- rest
and arsenic. He has sore throats every year. No excesses in food, drink, or
tobacco. Since becoming diabetic he has lost about 35 pounds weight. For
about a week past he has had pain in the great toe of the right foot.

Present Illness. — 3 years ago debility without other sjrmptoms began. The
urine was found to contain 5 per cent sugar. This gradually cleared up on
carbohydrate-free diet with addition of one sUce of bread at each meal. In 1913
he became worse and was placed in a hospital, where 3 green days cleared up gly-
cosuria. Since leaving the hospital he has constantly had 3 to 5 per cent sugar
in the urine. He continued work up to 4 months ago; since then he has been
physically and mentally incapacitated.

Physical Examination. — Sallow color; only moderate emaciation; acetone odor
present. Teeth in good repair. TonsUs and throat normal. Axillary glands

CASE RECORDS 297

palpable, but not cervical, epitrochlear, or inguinal. Arteries are palpably scler-
otic. Blood pressure 90 systolic, 75 diastolic. Knee jerks sluggish; Achilles jerks
active. The great toe of the right foot shows a slight abrasion. The toe is
bluish in color, cold to the touch, and the skin between it and the next toe is
lifted up by exudate. Examination otherwise negative.

Treatment.— There were 2 days of observation diet. On Feb. 13, the first full
day in hospital, this consisted of 84 gm. protein, 6 gm. carbohydrate, and 1830
calories. The glycosuria on this day was 31.3 gm., and the ferric chloride reac-
tion was strong. Fasting was then begun, particularly with a view to the in-
cipient gangrene. Whisky was permitted in quantities up to 500 calories of
alcohol. On Feb. 17, whisky was diminished to 30 cc, and 9 gm. carbohydrate
were added. Glycosuria, which had been absent, returned in traces and con-
tinued for 2 days longer, though the carbohydrate on Feb. 18 was diminished to
4 gm., and on Feb. 19 only whisky and 350 gm. thrice cooked vegetables were
given. These traces of glycosuria were accidental, or else continued undernutri-
tion brought rapid improvement; for beginning Feb. 20, 40 to 50 gm. carbo-
hydrate in the form of green vegetables were given daily without glycosuria,
vmtil Feb. 25. On Feb. 26, the carbohydrate was diminished to 10 gm. The
whisky was now 170 cc. Glycosuria ceased, but reappeared Mar. 3 on a diet
of 70 gm. protein and 1700 calories without carbohydrate. It became heavier
as the calories were increased to 2300, stopped with the fast-day of Mar. 7, re-
appeared with the carbohydrate-free diet of 2300 calories on Mar. 8, and ceased
when the diet was cut down to 1200 calories Mar. 9 to 11. There were no
vegetables of any kind in these later diets, so the glycosuria was evidently due
to the protein-fat intake. Thrice cooked vegetables were then added and were
at first tolerated, but glycosuria reappeared on Mar. 13, 14, and 15, on diets lower
in protein and calories than those formerly assimilated. Though the vegetables
on these days consisted only of 150 gm. string beans and 100 gm. celery, both
thrice boiled, the glycosuria was evidently due to this trifle of carbohydrate.
This very low tolerance improved with continued undernutrition and the dim-
inution of other elements in the diet. Thus, beginning Mar. 17, the same
thrice boiled vegetables were tolerated, the protein now being 30 gm. and the
total calories 400. This diet was gradually built up and on Apr. 3 a trace of
glycosuria appeared with 75 gm. protein, 200 gm. thrice boUed vegetables (string
beans and asparagus), and 1700 calories. This stopped on the fast-day of Apr.
4; and on Apr. 5, 5 gm. carbohydrate in the form of asparagus, celery, and lettuce,
without other food, were tolerated without glycosuria. Beginning Apr. 6 the
protein was diminished to 40 gm. and the calories to 1400. With this reduction
in protein, not only did the same quantity of thrice cooked vegetables cause no
glycosuria, but also on Apr. 9 and 10 the addition of 10 gm. carbohydrate was tol-
erated. The attempt during the ensuing week (Apr. 12 to 17) to raise the carbo-
hydrate to 20 to 30 gm. and the calories to 1800 resulted in slight glycosuria.
The tendency to glycosuria gradually diminished, and by July 7 the patient had

298 CHAPTER m

become able to tolerate 80 gm. protein, 25 gm. carbohydrate, and 2150 calories
(over 1.5 gm. protein and 40 calories per kg. for a weight of SO kg., but dimin-
ished one-seventh by the weekly fast-days). He was dismissed on this diet in
good condition.

Acidosis. — This was never acutely threatening. The ferric chloride reaction
was fairly persistent. It cleared up with the undernutrition at the close of Mar.,
and returned with the higher diets in Apr., even though carbohydrate was soon
added to these diets. Then, without special change in the diet, the ferric chloride
reaction gradually disappeared and was absent at discharge. 20 gm. sodium bi-
carbonate were given daily Feb. IS to 22. On Feb. 23, it was diminished to 5
gm., and then stopped. The carbon dioxide capacity of the plasma, as far as
observed after Mar. 18, was within or near normal Umits, and was high at
discharge.

Blood Sugar. — ^This fluctuated, but hyperglycemia was the rule. The last
analysis on June 24 still showed 0.165 per cent. It is evident that hyperglycemia
did not prevent continued improvement in tolerance and sjonptoms. Neverthe-
less, this hjrperglycemia is an unfavorable feature. It could doubtless have been
brought lower, but the patient was unintelligent and untrustworthy. For this
reason an ideal result was not considered possible in his case, and a fairly satis-
fying diet was therefore permitted, with some hope that improvement might stiU
be possible, if he remained continuously free from glycosuria.

Weight and Nutrition. — The rise of 5 kg. in weight from Feb. 15 to 23 was
due to edema resulting from the sodium bicarbonate. The weight fell rapidly on
stopping the bicarbonate. Beginning May 31 there was another onset of edema
independent of bicarbonate or other known cause. Albumin and casts were
absent from the urine. The entire gain in weight from May 31 to June 16 was 6
kg. That this was wholly due to fluid retention, apparently from renal cause,
is shown by the prompt fall following June 16, when salt-free diet was instituted.
The entire period in hospital represented undernutrition such that the weight was
diminished by 4 kg. There was clinical benefit instead of injury. Under the
fasting and subsequent treatment the threatened gangrene cleared up smoothly.
Strength was regained, the appearance and color improved, and at discharge the
patient was able to resume his work, in contrast to the state of incapacity at the
time of admission with higher weight and active diabetes present.

Subsequent History. — ^The patient followed diet and showed normal urine for
several months. In Aug. he passed through a severe bronchitis without show-
ing sugar. Toward Oct. he had much business worry, and analysis showed 0.204
per cent sugar in the whole blood and 0.278 per cent in the plasma (probably
more dietetic than psychic in origin, however). The patient rejected the advice
to return to the hospital at this time because of business emergencies which he
must meet. He again reported at the hospital on Nov. 29. Meantime he had
been traveling through other states under conditions which prevented following
diet. The blood sugar was 0.227 per cent, plasma sugar 0.244 per cent. He was

CASE EECOBDS 299

instructed as to becoming sugar-free at home, and on Dec. 5 reported that glyco-
suria had stopped with 1 day of fasting and had remained absent on his regular
diet. The urine on this date was normal, the blood sugar 0.208 per cent,^ the
plasma sugar 0.2S0 per cent. On Dec. 12 a trace of glycosuria appeared, and
the patient therefore fasted on Dec. 13. The urine was normal, the blood sugar
0.178 per cent, the plasma sugar 0.213 per cent. The patient was continually
inclined to carelessness, but felt worse when showing sugar and therefore made
some attempts at following diet. On Dec. 28 he returned to the hospital.

Second Admission. — ^The urine showed slight sugar and ferric chloride reac-
tions. On the observation diet of Dec. 29, comprising 77 gm. protein, 15 gm.
carbohydrate, and 2000 calories, a trace of glycosuria persisted in the early hours
but cleared up before the close of the day. A fast-day was nevertheless imposed
on Dec. 30, followed by a routine carbohydrate test, which fixed the tolerance at
70 gm. carbohydrate. On the subsequent diets entirely unaccountable traces of
glycosuria occurred, and the patient finally proved to be repeatedly violating
diet. On account of his persistent carelessness and disobedience, he was dis-
missed and was referred to a local speciahst, with the idea that he might appre-
ciate treatment more if he had to pay for it.

Remarks. — On the fast-day of Dec. 30 the blood sugar was 0.111 per cent and
the plasma sugar 0.122 per cent. It is seen that the body weight at the second
admission was identical with that at the former discharge. Notwithstanding
repeated indiscretions in carbohydrate, the patient had kept down his total diet
approximately as directed, and the tendency to a lowering of the hyperglycemia,
as hoped for at the previous discharge, had actually shown itself. The case had
been characterized by very low tolerance in the initial period of the first admission,
but, in consequence of the undernutrition then imposed, had become easy to man-
age. The only difficulty was the light-mindedness of the patient. He was dis-
charged in favorable clinical condition, with prognosis governed by behavior.

CASE NO. 32.

Female, married, age 21 yrs. Russian Jew; housewife. Admitted Feb. 18,
1915.

Family History. — Father died when patient was an infant. Mother well at
51. One brother and one sister well. No heritable disease known.

Past History. — Considerable sickness in infancy. Diphtheria complicated by
measles at 2i years. Pneumonia at 3 years. Healthy life since then. Habits
regular. Diet largely carbohydrate, but no sugar. Married 3 years, has a
healthy 2 year old child. The only recent illness was a 2 day attack of tonsil-
litis 2 years ago.

Present Illness.— Last June began polyphagia, polydipsia, polyuria, weakness,
headache, and pains in legs. Recently pruritus vulvae. Menstruation stopped
last Oct. Patient supposed all the symptoms due to pregnancy, and was sur-
prised when a physician found pregnancy absent and diagnosed diabetes. She
was sent to this hospital for impending coma.

300 CHAPTER ni

Physical Examination. — Height 168.5 cm. A well developed and nourished
young woman, with flushed face and drowsy expression. Dyspnea is present;
respiration about 30 per minute. Teeth in fair condition; some pyorrhea. Ton-
sils moderately hypertropMed; the left axillary and epitrochlear glands pal-
pable; cervical and inguinal not palpable. Knee jerks not obtainable; Achilles
jerks present. Blood pressure 100 systolic, 65 diastolic. Faint albuminuria.

Treatment. — Because of the imminent danger of coma, fasting was begun im-
mediately, with some 400 to 600 calories of whisky daily. Th^ patient was con-
scious though sleepy, and not nauseated. On Feb. 18 she received 10 gm.
sodium bicarbonate and 2 gm. compound jalap powder; 30 gm. sodium bicarbon-
ate on Feb. 20 and 21,10 gm. on Feb. 22. She was thirsty, and was able to drink
as much as 3 liters of water daily, but the main reliance was placed on fasting.
Both the glycosuria and the clinical symptoms rapidly cleared up. The urine
became neutral on Feb. 21. Glycosuria was absent on Feb. 23, but the first food
was allowed on Feb. 26. This consisted only of 12 gm. carbohydrate in the form
of green vegetables. By Mar. 6 it had been increased to 50 gm. carbohydrate
without glycosuria. The whisky meanwhile was continued at 500 calories daily.
It might have been well to have pushed the carbohydrate to the point of glycosuria,
with a view to clearing up the remaining slight ferric chloride reaction. But
after the fast-day with whisky on Mar. 7, protein-fat diet was begun. On Mar.
10 whisky was permanently stopped. The diet was gradually built up to 118
gm. protein, 25 to 27 gm. carbohydrate, and 2600 to 2800 calories (approximately

2.4 gm. protein and 52 to 56 calories per kg. on 50 kg. weight, reduced one-seventh
by the weekly fast-days), with only transient traces of glycosuria. She was
dismissed Apr. 7 on a diet of 85 gm. protein, 20 gm. carbohydrate, and 2500 cal-
ories (1.7 gm. protein and 50 calories per kg. reduced by weekly fast-days to

1.5 gm. protein and 43 calories average). This was weU below what she had
seemed able to tolerate. At discharge she was to all appearances entirely healthy.

Acidosis. — ^The carbon dioxide capacity of the plasma was only 26.4 vol. per
cent at admission. Fasting was evidently the most important factor in raising it,
for on Feb. 19, after only 10 gm. sodium bicarbonate, it had risen to 38.5 per
cent. Under the larger doses of bicarbonate it rose still more rapidly to the
high normal figure of 64.6 per cent on Feb. 22. This was an artificial elevation
resulting from the alkali dosage, for with discontinuance of alkali the COa ca-
pacity fell steeply to 45 per cent on Feb. 25. Under the influence of the small
quantities of carbohydrate it rose spontaneously within normal limits, reaching
62.2 per cent on Mar. 4, without the aid of alkali. It fell on the fast-day of Mar.
7, alcohol alone being apparently unable to hold it up. It continued to fall, on
addition of protein and fat, down to 46.5 per cent on Mar. 10. The steep rise to
56 per cent on Mar. ll and 60 per cent on Mar. 12 is perhaps explainable by the
introduction of 75 gm. protein in the diet. From this time the curve tends to
run near or slightly below the lower normal limit, and was barely at this limit
at discharge. The ferric chloride reaction was intense at the outset, diminished

CASE RECORDS 301

rapidly during the fast, and was down to traces during the ensuing carbohydrate
period. The later diet being a high one, this reaction did not become perma-
nently negative in hospital. Notwithstanding the use of alkali, the ammonia
nitrogen on Feb. 19 was up to 3.54 gm. It fell as steeply as the plasma bicar-
bonate rose. Its general course was still downward after discontinuance of
alkali, but with the beginning of protein-fat diet, as the CO2 capacity fell, the
ammonia again rose, up to 1.9 gm. N on Mar. 11, with a fall thereafter, perhaps
partly because of introduction of carbohydrate, perhaps partly because of the
improved condition. No clinical symptoms were associated with the persistent
traces of ferric chloride reaction and chronically low CO2, and the use of alkali
was not indicated.

Blood, Sugar. — ^This was down to 0.128 per cent on the morning of Mar. 22,
following the preceding fast-day. On Apr. 3, at the close of a week of high diet,
it was up to 0.192 per cent. Following the fast-day of Apr. 4, the blood sugar
on the morning of Apr. 5 was found to have returned promptly to the normal
level of 0.117 per cent. At discharge on Apr. 7 it was 0.133 per cent. It could
have been kept rigidly within normal limits, but a gradual fall was hoped for
with continued improvement under suitable diet.

Weight and Nutrition. — ^The initial fall in weight during fasting was moderate,
amounting to 2 kg. in 8 days. The bicarbonate did not produce edema, but
beginning Feb. 26 the green vegetables produced a definite water retention, as
often happens, so that the weight on Mar. 2, after practically continuous fasting,
was 1 kg. higher than at admission. This slight but visible edema cleared up
spontaneously and did not return. It wUl be noted that the initial fasting
treatment, which cleared up the impending coma, consisted in 18 days of total
abstinence from food, except the moderate quantities of alcohol and trifle of
green vegetables. The weight fell from 53.2 kg. on Feb. 18 to 49 kg. on Mar.
9, a loss of 4.2 kg. Later with higher diets it tended to rise slightly, but was
only 50 kg. at discharge; i.e., 2.3 kg. less than at admission. It was hoped that
the case was mild enough to permit a moderate gain in weight, and as the patient
had to work, a liberal diet was allowed as described.

Subsequent History. — ^This patient, though poor and uneducated, adhered
strictly to dietary instructions. The urine was continuously free from sugar
and the ferric chloride reaction had disappeared, therefore lO gm. carbohydrate
were added to the diet on May 26. On June 4, the blood sugar was 0.105 per
cent; on June 11, 0.122 per cent in the whole blood, 0.143 per cent in the plasma.
The weight had risen to 56.3 kg. By Oct. 12, it had risen to 62.3 kg. The blood
sugar then was 0.130 per cent and the CO2 capacity of the plasma 66.2 vol. per
cent. The diet was then increased by 200 cc. milk, as the patient reported her-
self not yet quite up to full workiiig strength. On Nov. 3, the sugar in the
blood was 0.149 per cent, in the plasma 0.175 per cent, and the CO2 capacity was
56.3 per cent.

On Nov. 22, the sugar in the blood was 0.130 per cent, in the plasma 0.143

302 CHAPTER III

per cent, and CO2 capacity 42.5 per cent. The first trace of sugar was reported
in the urine.

On Dec. 6, the patient reported having had cold and cough for 10 days. The
urine remained normal, and she probably ate less than usual, for the sugar was
found to be 0.100 per cent in the blood, 0.105 per cent in the plasma; the CO2
capacity 65.5 per cent.

On Dec. 23, the patient reported at the hospital with fever of 100°, com-
plaining of pains in joints and chest. She continued to feel badly and lost a
few pounds in weight. The urine remained normal. Her menstruation, which
had returned in the autumn, had again ceased.

On Dec. 27, she was readmitted because of her cold or grippe, though diabetic
symptoms were absent.

Second Admission. — Coryza was present, but the general appearance was good.
Temperature was never above 99.8°F. The body weight was now 58.3 kg., as
compared with 53.2 kg. at the first admission. Glycosuria was present Dec.
29 to 31, on a diet of 90 gm. protein, 50 gm. carbohydrate, and 2075 calories (1.54
gm. protein and 35.6 calories per kg.). The low blood sugars recorded mornings
before breakfast show the absence of any continuous hyperglycemia. The am-
monia nitrogen was 0.73 gm., and the total acidity (Henderson) 205. A carbo-
hydrate tolerance test was instituted in the usual manner, beginning with a fast-
day on Jan. 2. The increase in carbohydrate was made more rapidly than usual
because of the high tolerance, which was found to be approximately 180 gm.
carbohydrate. The patient was discharged on Jan. 16, 1916, weighing 57.8 kg.,
with a prescribed diet of 100 gm. protein, 50 gm. carbohydrate, and 2000 calories
(1.7 gm. protein and 35 calories per kg., reduced one-seventh by the weekly
fast-days). She was advised this time to take as much open air exercise as pos-
sible in order to buUd up her strength and relieve her chronic neurasthenia. The
blood sugar had now come down to normal, so that all tests were normal in all
respects, and the physical condition was entirely favorable.

Subsequent History. — The patient remained free from glycosuria and acidosis,
notwithstanding an attack of tonsillitis in Mar. Normal menstruation returned
in Apr. In July she again had fever and a grippe-Uke iUness.

Third Admission. — On account of this she was readmitted on July 13, 1916,
with definite tonsillitis and temperature of 100.5° F. This cleared up in a few
days. The general condition was good, and the weight 54.5 kg. A carbohydrate
test at this time showed a tolerance of 190 gm.; i.e., practically identical with the
180 gm. half a year before. The patient was discharged on Aug. 15, 1916, weigh-
ing 52.2 kg., with a prescribed diet of 90 gm. protein, 60 gm. carbohydrate, and
2300 calories.

Subsequent History. — ^The urine remained normal. On Aug. 29, the blood sugar
was 0.2 per cent, the plasma sugar 0.204 per cent, CO2 capacity 65.1 per cent.
On Sept. 6, the blood sugar was 0.167 per cent, the plasma sugar 0.181 per cent,
the COa capacity 65.8.

CASE RECORDS 303

Fourth Admission.— On Oct. 24, 1916, the patient was again admitted to hos-
pital because of cold and sore throat. The urine was normal, but a carbohy-
drate test showed a tolerance of only 130, as compared with the former 190 gm.
She was again discharged on Dec. 5, 1916, in good physical condition, on a diet of
75 gm. protein, 30 gm. carbohydrate, and 1750 calories. Her weight was 51.6
kg. The blood sugar was 0.164 per cent.

Fifth Admission. — Feb. 20, 1917. The trouble again was tonsillitis with fever.
There had been increasing tendency to glycosuria following repeated attacks of
sore throat, and the patient had recently carried out a carbohydrate test in the
regular manner at home, which showed a tolerance of only 90 gm. carbohydrate.
A test prior to this had shown a tolerance of only 70 gm. carbohydrate. The
general condition was still good, but the patient was kept in hospital for some
time in order to prepare her for tonsillectomy under the most favorable conditions.
Tonsillectomy was performed under local anesthesia on Mar. 19, 1917, and
was followed by no glycosuria, acidosis, or complication of any kind.

The patient was discharged Apr. 6, 1917, on a diet of 50 gm. protein, 10 gm.
carbohydrate, and 1200 calories, weighing 46.5 kg.

Subsequent History. — On a low diet, made still lower by weekly fast-days, the
urine remained normal and the patient felt well except for weakness. There were
no more sore throats, bm occasional joint pains returned as in the previous
attacks.

By May 22, the diet was increased to 55 gm. protein, 10 gm. carbohydrate,
and 1500 calories. On June 5, it was further increased to 60 gm» protein, 10
gm. carbohydrate, and 1600 calories. The weight was 46.5 kg.

On June 19 the blood sugar was 0.161 per cent and the CO2 capacity 61.7 per
cent. On account of complaints of persistent weakness and recurrent attacks of
so called rheumatism, the diet was further increased to 75 gm. protein and 1800
calories (1.6 gm. protein and 38.5 calories per kg.). On July 3, the weight was
47.3 kg., the blood sugar 0.172 per cent, the CO2 capacity 58.4 per cent. The
general condition seemed slowly but steadily improving.

Remarks. — ^This result, 2^ years after the patient was first received on the
verge of coma, is not bad under the circumstances. Downward progress, though
not rapid, has been perceptible in the presence of two distinct causes.

The first to be considered is diet. In the light of later experience a severely
diabetic patient, aged 21 years, ought not to receive an average ration of 43 cal-
ories per kg. as prescribed for this patient at the first discharge. One of the
hopeful features of the earher stage of diabetes is the abiUty to react energetically
and to carry even unduly high diets with apparent safety for a considerable
length of time. The most discouraging feature of the later stage resulting from
these high diets is the apparent breakdown of recuperative power, so that lower
diets may then spare the weakened assimilation, but can no longer raise it. This
patient at her first discharge had good flesh and color, but was hindered in earn-
ing her living by slight neurasthenia and subjective weakness. The familiar

304 CHAPTER in

attempt was therefore made to build her up by liberal feeding. For a time she
displayed the ability, characteristic of this incipient stage, to carry the increase of
both diet and weight; but the neurasthenia was not cured, nor the recurrent in-
fections prevented. It is apparent that the high diet had the usual eflfect of low-
ering the assimilation and weakening the power of recovery. Evidence is seen
in the marked hyperglycemia on certain occasions between the first and second
admissions, and in the persistent traces of glycosuria, Dec. 29 to 31, 1915, on diets
lower than had been tolerated at the close of the first admission. At the second
admission the blood sugar was kept normal. In contrast to the former 2500
calories, she was discharged this time on the wiser diet of 2000 calories (30 cal-
ories per kg. daily average). The third admission was 7 months later, and the
carbohydrate tolerance test proved that no loss of assimilation had occurred dur-
ing this interval. The diet -was then raised to 2300 calories. Marked hyper-
glycemia was found within 2 weeks; and in the interval of only 2 months between
the third and fourth admissions there was a demonstrated loss of 60 gm. carbo-
hydrate tolerance. The hyperglycemia at the fourth admission was not over-
come, and though the diet at discharge was only 1750 calories, traces of glycosuria
recurred and downward progress accordingly became more rapid. It is the fa-
miliar story that high diet first fails to accompUsh the intended purpose, and
subsequently forces the employment of lower diets than would have been proper
in the first place.

A second and highly important factor was that of infection. The attacks
recurred at all periods. The history shows, first, that high feeding did not pre-
vent the infectious attacks; second, that glycosuria and lowering of tolerance
from these attacks were most marked when the diet was unsuitable. Even if the
diet, however, had been perfectly planned, downward progress might still be
expected from the repeated infections. The comparative safety with which
operations can be performed with suitable preparation renders them advisable
in preference to a continuance of the infectious injury.

CASE NO. 33.

Female, married, age 51 yrs. Russian Jew; housewife. Admitted Feb. 18'
1915.

Family History. — ^Not much known. One sister died of consumption. Pa-
tient has been married 32 years; had eight children; one died after tonsillectomy;
others are well.

Past History. — Patient was bom in Russia. For past 9 years has lived in New
Jersey in good environment. Healthy life. Measles and typhus in childhood.
Had nervous breakdown at time of her son's death, and about that time all her
teeth became loose and were pulled out. During her first pregnancy she appears
to have had an acute nephritis following a cold; another such attack occurred last
year. Occasional indigestion and constipation. No alcoholism. Much starch
and sweets in diet. She has been obese throughout her adult life.

CASE RECORDS 305

Present Illness. — Over 2 years ago, because of nervousness, weariness, cold feet,
headache, and pains in limbs, she consulted a physician and diabetes was diag-
nosed. Glycosuria cleared up on carbohydrate-free diet; she did not reUsh it and
lost 25 pounds. Toast was then added to the diet, and later she was allowed even
cake. She regained 7 pounds weight and glycosuria returned. She was then re-
stricted to three slices of bread at each meal, but as glycosuria continued, the
suffering from the above symptoms was so great and continuous that she was
eager to submit to the most radical treatment if relief were obtainable.

Physical Examination. — ^Height 130 cm. A short, obese woman without acute
symptoms. General sensitiveness to touch. Skin of face pits slightly on pres-
sure. Teeth all false. Throat normal. No lymph node enlargement. Slight
emphysema. Systolic murmur at heart apex, transmitted to axilla. Blood
pressure 190 systolic, 100 diastolic. Knee jerks exaggerated. Ankles pit slightly
on pressure. Faint albuminuria without casts.

Treatment. — The patient was first placed on a low diet of approximately 52
gm. protein, 5 gm. carbohydrate, and 750 to 800 calories. With this intake the
glycosuria on Feb. 18 was 6.1 gm., and on Feb. 19, 5.95 gm. On the first day
of fasting (Feb. 20) it fell to 1 gm. and after a trace on Feb. 21, cleared up en-
tirely. For the purpose of reducing the excessive weight, plain fasting was con-
tinued for 1 week, with only 150 cc. cofifee and 150 cc. soup daily (Feb. 20 to 26).
On Feb. 27 and 28, nothing but whisky was given (250 to 400 calories), and then
green vegetables added, containing 12.5 gm. carbohydrate on Mar. 1 and in-
creasing to 50 gm. carbohydrate on Mar. 6. A fast-day with 300 calories of whisky
on Mar. 7 cleared up the resultant trace of glycosuria. Eggs and a trifle of crisp
bacon were then added to the whisky, but the total intake was not above 850
calories (Mar. 9). The trace of glycosuria which appeared on this day was prob-
ably attributable to 100 gm. string beans and 150 gm. cabbage, both thrice
boiled. This glycosuria cleared up on the following day on practically the identi-
cal diet. After Mar. 12 no more whisky was used, except on the fast-day of
Mar. 21. On Mar. 12 to 13, a diet of 25 to 40 gm. protein and approximately
300 calories was tolerated. But on Mar. 14, 68 gm. protein, 9 gm. carbohydrate,
and 1200 calories caused glycosuria, which continued on the subsequent days with
reduced caloric intake; the glycosuria was, however, very faint and ceased spon-
taneously on Mar. 20. The plan was pursued of giving a diet adequate in protein,
with carbohydrate to the limit of tolerance, but poor in fat and calories. Thus,
toward the early part of Apr. this diet contained about 120 gm. protein, 20 to 45
gm. carbohydrate, and 1000 to 1100 calories. Fast-days, sometimes doubled,
were given almost every week for reducing weight. Toward the close of Apr.
the patient had become able to assimilate as much as 118 gm. protein, 30 to 50
gm. carbohydrate, and 2000 calories. She never complained much of hunger
and was well satisfied on the later diets.

There was a general gain in clinical condition, but still many complaints of
headache and pains in abdomen and various parts of body. Weakness and ner-

306 CHAPTER m

vousness were also persistent. About the middle of Mar. occurred the first
menstruation since 8 months before admission to hospital. In Apr. there was
another menstruation, with undue hemorrhage. Gynecological examination
failed to reveal fibroids or other cause of hemorrhage, but some abnormality was
suspected because of the history of a similar trouble in the past. The patient was
discharged May 8, with the idea of having her reduce her weight further at
home and find something to divert her attention from her symptoms, which
were of the sort called neurasthenic. She was well pleased with the improvement
and could be trusted to continue treatment.

Acidosis. — ^A salient point is the absence of any threatening symptoms in this
obese woman during a week of complete fasting without special preparation. The
ferric chloride reaction, which had been negative, became positive on the low diet
of Feb. 19 and grew heavy during the fast. Alkali was not employed. The ferric
chloride reaction subsequently diminished, but was not permanently negative
during this period in hospital. In the latter part of the stay in hospital the
ammonia followed a fairly low curve, and the plasma bicarbonate held a low
normal level.

Blood Sugar. — There is little to remark except the downward tendency. Evi-
dently radical measures might have brought it within normal limits rather quickly,
but in view of the general condition it was deemed preferable to allow the hyper-
glycemia to be taken care of in the course of long improvement.

Weight and Nutrition. — The most important therapeutic purpose was to di-
minish the excessive body weight. The abdomen was very pendulous, and the
question- arose whether there might not be benefit from a surgical operation which
should correct the diastasis of the recti and tighten up the abdominal wall, per-
haps thereby relieving some neurasthenic complaints, and at the same time am-
putate some 10 or 15 pounds of fat which were sufficiently in the patient's way
that she would have welcomed surgical relief. It was decided not to venture this,
but to depend entirely on dietary measures. The weight fell rapidly on fasting,
and continued to fall on the subsequent diet which conformed to the above men-
tioned standard of adequate protein, carbohydrate to the limit of tolerance, and
restriction of fat. The weight at admission was 83 kg., at discharge 70.6 kg.;
i.e., a loss of 12.4 kg. in 2| months. The discharge diet represented 92 gm. pro-
tein, 30 gm. carbohydrate, and 1800 calories (approximately 1.3 gm. protein and
25 calories per kg., reduced one-seventh by the weekly fast-days). As usual, the
clearing up of diabetic symptoms by reduction of weight had resulted in actual
gain of strength. In this instance the reduction of the obesity was in itself a reUef
to the patient.

Subsequent History. — The presence of a somewhat elevated blood pressure and
the occasional uterine hemorrhages raised a question in regard to exercise in this
patient. She was advised to practice walking and to work 3 or 4 hours every day
in her garden. The urine continued to show negative sugar and slight ferric
chloride reactions. On June 11, the diet was increased by 50 gm. meat, 2 eggs,

CASE RECORDS 307

and 10 gm. carbohydrate. The weight was 70 kg. On July 21, the carbohy-
drate intake was increased to 50 gm., and at the same time the fat was dimin-
ished by omitting 25 gm. olive oil. Though the condition in respect to diabetes
remained uniformly good, the patient's neurasthenia made her a nuisance to a
devoted family, and she was therefore readmitted to the hospital on Aug. 25 for
observation.

Second Admission. — ^The sugar was down to 0.112 per cent in the blood, 0.118
per cent in the plasma. A slight ferric chloride reaction still persisted. None
of the organic disorders suggested by the patient's numerous complaints could be
found. She was again kept on very low diet, the fat being particularly low, the
protein low but adequate as before, and in this instance the carbohydrate was
also made low with the idea of maintaining a normal blood sugar. This was
also the diet prescribed at discharge; namely, 100 gm. protein, 10 gm. carbohy-
drate, and 1000 to 1100 calories. The patient was now some 7 kg. below the
weight at her former discharge, and the loss was expected to continue.

Subsequent History. — The progress was as before. Glycosuria remained absent,
and on Oct. 6 the ferric chloride reaction was also found negative. Hyperglycemia
was, however, found to be present after eating, the sugar being 0.156 per cent in
the whole blood and 0.182 per cent in the plasma. The varied neurasthenic com-
plaints had diminished but were stiU upsetting the patient herself and her entire
household. There had been no recurrence of the former uterine hemorrhages,
and the patient was readmitted to hospital on Oct. U to try more vigorous exercise
under supervision.

Third Admission. — The weight was down to 59.2 kg.; i.e., a loss of 24 kg.
since the first admission. The patient was far stronger and more cheerful.
Both sugar and ferric chloride reactions were negative. A carbohydrate test
was now begun in routine manner with a fast-day on Oct. 11, then green vege-
tables with increase of carbohydrate by 10 gm. daily. A slight ferric chloride
reaction quickly reappeared and persisted until abolished by increase of carbo-
hydrate; i.e., with the ingestion of 80 gm. carbohydrate on Oct. 21. The trace
of glycosuria appearing with the 150 gm. carbohydrate on Oct. 29 was evidently
accidental, for it disappeared with further increase of the ingestion, and the true
limit seemed to be reached with 250 gm. carbohydrate Nov. 7 to 13. This assimi-
lation is in striking contrast to the almost complete absence of tolerance shortly
after the first admission. One contributing factor in it seemed to be exercise
(see Chapter V) . The slight glycosuria was cleared up by a fast-day on Nov. 14,
which promptly brought the high blood sugar of the carbohydrate test down to
0.119 per cent in the whole blood and 0.125 per cent in the plasma. Thereafter
a trial was made of a diet of 75 gm. protein, 150 gm. carbohydrate, and 2500
calories. Persistent traces of glycosuria resulted, evidently from the carbohy-
drate, inasmuch as the blood sugar curve shows normal values in the morning
before breakfast. The carbohydrate was therefore diminished to 100 gm., and
the intake of 2500 calories maintained by substituting fat. The patient was dis-
charged on Nov. 26, 1915, weighing 55.6 kg., a total loss of 27.4 kg. since her first

308 CHAPTER in

admission. Her diet now represented approximately 1.3 gm. protein and 45 calo-
ries per kg., reduced one-fourteenth by fortnightly fast-days. The exercise had
been strenuous during this period in hospital, and it proved wholly beneficial.
She had reached a point where she could walk 8 mUes and climb 40 flights of stairs
daily in addition to an hour or two of jumping rope and tossing the medicine
ball. A fairly liberal diet was therefore allowed at the close to maintain strength
and nutrition and furnish energy for exercise.

Subsequent History. — On Dec. 13, 1916, the weight was 60 kg., and the patient
was doing her full housework and walking 5 miles and using a 6 potmd medicine
ball half an hour daily, with almost complete relief from neurotic troubles. In
summer, gardening was largely substituted, and she spent 6 hours daily at this
work.

On Jime 15, 1916, sugar was 0.141 per cent in the whole blood, 0.185 per cent in
the plasma; CO2 capacity 63.5 per cent; weight 52 kg. The patient complained
somewhat of himger, and on July 22 the diet was changed to 100 gm. protein, 50
gm. carbohydrate, and 2750 calories. On this diet the sugar was 0.159 per cent
in whole blood, 0.192 per cent in plasma, CO2 capacity 57.9 per cent. Blood
pressure 130 systolic, 90 diastolic.

In Sept., the weight was 54 kg. Occasional doubtful traces of glycosuria were
reported, but on examination at the hospital such reactions were found to be
false, the slight sediment not representing a true copper reduction. Prog-
ress has continued in this manner to the present. Neiirasthenic symptoms stiU
persist to some extent, pain being complained of at different times in head, abdo-
men, legs, and fingers. The quantity of the diet is fuUy satisfactory. Monot-
ony is sometimes complained of. Active work is still continued with pleasure,
and in general the patient is entirely transformed in health and appearance as
compared with her first admission.

Remarks. — There are three salient points. First is the good toleration of fast-
ing by an obese woman without symptoms of acidosis, and the improvement in
strength with undernutrition. Second is the transformation produced in the
sugar tolerance by reduction of weight, an increase from practically zero to 250
gm. Third is the beneficial effect of exercise in a patient apparently showing some
contraindications. The dangers feared did not materialize, and even the blood
pressure came down to normal. There is still an abundant supply of body fat,
but undoubtedly a larger proportion of the weight is now muscle. The neuras-
thenia was benefited more than the carbohydrate tolerance, and without exercise
it is doubtful if permanently favorable results could have been achieved.

CASE NO. 34.

Male, unmarried, age 26 yrs. Jew; clerk. Admitted Feb. 19, 1915.

Family History. — Father well at 55. Mother died with diabetes and cardio-
renal disease at 51. Two brothers and three sisters are well; one brother died in
infancy; one sister died this year in diabetic coma, aged 19. No knowledge tf
other heritable disease.

308 CHAPTER III

admission. Her diet now represented approximately 1.3 gm. protein and 45 calo-
ries per kg., reduced one-fourteenth by fortnightly fast-days. The exercise had
been strenuous during this period in hospital, and it proved whoUy beneficial.
She had reached a point where she could walk 8 miles and climb 40 flights of stairs
daily in addition to an hour or two of jumping rope and tossing the medicine
ball. A fairly liberal diet was therefore allowed at the close to maintain strength
and nutrition and furnish energy for exercise.

Subsequent History.— On Dec. 13, 1916, the weight was 60 kg., and the patient
was doing her fuU housework and walking 5 nules and using a 6 pound medicine
ball half an hour daily, with almost complete relief from neurotic troubles. In
summer, gardening was largely substituted, and she spent 6 hours daily at this
work.

On June 15, 1916, sugar was 0.141 per cent in the whole blood, 0.185 per cent in
the plasma; CO2 capacity 63.5 per cent; weight 52 kg. The patient complained
somewhat of hunger, and on July 22 the diet was changed to 100 gm. protein, 50
gm. carbohydrate, and 2750 calories. On this diet the sugar was 0.159 per cent
in whole blood, 0.192 per cent in plasma, CO2 capacity 57.9 per cent. Blood
pressure 130 systoUc, 90 diastolic.

In Sept., the weight was 54 kg. Occasional doubtful traces of glycosuria were
reported, but on examination at the hospital such reactions were found to be
false, the slight sediment not representing a true copper reduction. Prog-
ress has continued in this manner to the present. Neurasthenic symptoms still
persist to some extent, pain being complained of at different times in head, abdo-
men, legs, and fingers. The quantity of the diet is fuUy satisfactory. Monot-
ony is sometimes complained of. Active work is stUl continued with pleasure,
and in general the patient is entirely transformed in health and appearance as
compared with her first admission.

Remarks. — There are three saUent points. First is the good toleration of fast-
ing by an obese woman without symptoms of acidosis, and the improvement in
strength with undernutrition. Second is the transformation produced in the
sugar tolerance by reduction of weight, an increase from practically zero to 250
gm. Third is the beneficial effect of exercise in a patient apparently showing some
contraindications. The dangers feared did not materialize, and even the blood
pressure came down to normal. There is still an abxmdant supply of body fat,
but undoubtedly a larger proportion of the weight is now muscle. The neuras-
thenia was benefited more than the carbohydrate tolerance, and without exercise
it is doubtful if permanently favorable results could have been achieved.

CASE NO. 34.

Male, immarried, age 26 yrs. Jew; clerk. Admitted Feb. 19, 1915.

Family History. — Father well at 55. Mother died with diabetes and cardio-
renal disease at 51. Two brothers and three sisters are well; one brother died in
infancy; one sister died this year in diabetic coma, aged 19. No knowledge •f
other heritable disease.

CASE RECORDS 309

Past History. — ^Healthy life in fair environment. Measles in childhood, the
only sickness. Venereal denied. No excesses in alcohol or tobacco. Diet
moderate without much sweets, but has consisted largely of bread and meat; few
vegetables.

Present Illness. — In Nov., 1911, the patient consulted a physician for pains in
his arms. Local examination revealed nothing, and a liniment was prescribed
which accomplished nothing. An osteopath was then consulted and gave elec-
trical treatments without result. In the latter part of 1912 the patient returned
to the original physician, who this time discovered glycosuria. On carbohydrate-
free diet plus one slice of Graham bread daily, glycosuria diminished. The
physician sent the patient to a sanitarium, where he remained 5 weeks. Glyco-
suria was absent only on green days, but the patient returned home with sugar
diminished and strength improved. He resumed work as a clerk, but gradually
became worse, and in 1913 was again sent to the sanitarium. Glycosuria did not
cease and the result was less favorable. He attempted light work after return-
ing home, but becoming alarmed by the downward progress, with polyphagia and
polydipsia, he spent S weeks under the care of Carl von Noorden in the summer
of 1914. He was free from glycosuria only on 1 fast-day, but felt improved in
strength on leaving. He resumed light work on carbohydrate-free diet with addi-
tion of 250 to 300 calories carbohydrate.

Physical Examination. — ^A well developed young man, thin, but not seriously
emaciated. No acute symptoms or distress. Flush of cheeks and slight yellow-
ish color about nasolabial folds. Teeth in good repair; throat slightly congested;
tonsils not hypertrophied. No palpable lymph node enlargements. Blood
pressure 110 systolic, 90 diastolic. Knee jerks active. Examination otherwise
negative.

Treatment. — On admission, the patient had glycosuria of 6.61 per cent or
150 gm. in 17 hours, with an intense ferric chloride reaction. There were no
symptoms suggesting coma, and no hesitancy was felt in instituting carbohy-
drate-free diet. On Feb. 20 and 21 the diet was 75 to 80 gm. protein, 2 to 3 gm.
carbohydrate, and 1650 to 1750 calories. The glycosuria fell to 33.2 gm. on
Feb. 20, and 18.65 gm. on Feb. 21. Fasting was then begun with 500 to 600
calories of whisky daily. On Feb. 25 the urine was free from sugar and the
ferric chloride reaction was much diminished. On Feb. 27, green vegetables were
added to the whisky, and increased to 100 gm. carbohydrate on Mar. 7 to 8. A
trace of glycosuria then appeared, whUe a slight ferric chloride reaction still
persisted. After a fast-day with 600 calories whisky on Mar. 9, two eggs and 20
gm. bacon were added, and increased to a total of 1300 calories on Mar. 11.
Whisky was then dropped and carbohydrate introduced; but the diet of 91 gm.
protein, 25 gm. carbohydrate, and 1740 calories on Mar. 13 to IS proved de-
cidedly in excess of the tolerance. After a fast-day on Mar. 16, a low carbohy-
drate-free diet was again begun. On Mar. 24, it became possible to introduce
10 gm. carbohydrate. The diet was then progressively built up until before

310 CHAPTER ni

discharge on May 8, it represented 95 gm. protein, SO gm. carbohydrate, and
2900 calories. The diet prescribed at discharge was 80 gm. protein, 10 gm. car-
bohydrate, and 2500 calories (nearly 1.6 gm. protein and 50 calories per kg.,
reduced one-seventh by weekly fast-days). The patient looked entirely weU and
described himself as feeling better than at any time since the onset of diabetes
He was discharged to rest in the country during the summer.

Acidosis. — There were no threatening s)rmptoms, either on carbohydrate-free
diet, or during the initial fast. The carbon dioxide capacity of the plasma was
slightly below the lower normal level at admission, but rose spontaneously and
was normal toward the close of the stay in hospital. No alkali was employed at
any time. The chief signs of acidosis were the ammonia nitrogen of 3.1 gm. at
admission, and the intense ferric chloride reactions. The ammonia fell rapidly
to normal values. The beginning of a diet deficient in carbohydrate brought it
up to 1.4 gm. N on Mar. 12, but later the curve ran lower. The ferric chloride
reaction gradually diminished and was sometimes negative, but never remained
so during this hospital period.

Blood Sugar. — On Mar. 24, without glycosuria, there was nevertheless a fasting
blood sugar of 0.23 per cent. On Mar. 29, following the preceding fast-day, the
morning blood sugar was 0.17 per cent. Thereafter the findings were all below
0.2 per cent. The normal blood sugar on Mar. 3, after the preceding fast-day,
indicated a downward tendency, and showed that more rigorous treatment could
easily have maintained a normal level.

Body Weight. — ^This was 51.6 kg. at admission. The lowest figure, on Mar. 29
and Apr. 5, was 48.2 kg., representing a loss of 3.4 kg. There was occasional
slight edema, and particularly during the initial fasting and carbohydrate period
up to Mar. 8 there was pronounced edema with gain of 0.5 kg. in weight. The
weight rose on the higher diets in Apr. and May, and at discharge was 51.2 kg.;
«. e., 0.4 kg. less than at admission.

Subsequent History. — ^Intelligence and financial circumstances were in the pa-
tient's favor. He adhered to diet while resting in the country, but on May 18
showed glycosuria, and as the traces did not clear up he fasted 48 hours. On
May 25, his urine showed positive sugar and negative ferric chloride reactions.
The diet was quantitatively reduced, and thereafter glycosuria remained absent
except for traces appearing at the close of each week and cleared up by the
routine fast-days. He was therefore readmitted to the hospital on July 28.

Second Admission. — ^Almost 1 kg. had been gained since the former discharge,
so that the patient now weighed 0.4 kg. more than at the previous admission.
The urine was sugar-free but showed a well marked ferric chloride reaction. A
carbohydrate tolerance test was first instituted. Beginning with a fast-day on
July 28, 20 gm. carbohydrate in the form of green vegetables were given on July
29 and increased 20 gm. daily until well marked glycosuria occurred with an in-
take of 120 gm. After a fast-day on Aug. 5, the diet on Aug. 6 and 7 con-
sisted of 100 gm. protein, 30 gm. carbohydrate, and 2580 calories. Glycosuria

CASE RECORDS 311

resulted; also the ferric chloride reaction, which had become negative during the
carbohydrate test, returned. A lower diet was then begun, of SO gm. protein, 10
gm. carbohydrate, and 1300 calories. It became possible to increase the carbohy-
drate to 20 gm., and the ferric chloride reaction became negative. Sept. 9 to 11
the patient was at home on this same diet. Sept. 12 was a fast-day. A diet of SO
gm. protein, 70 gm. carbohydrate, and 1200 to 1400 calories then caused well
marked glycosuria. The fast-day of Sept. 18 was spent at home. The same
carbohydrate was given for the following week and strenuous exercise begun.
Glycosuria remained absent during this week, though the protein was increased
to 80 gm. and the calories to 2030. Sept. 27 to Oct. 9, a diet of 80 gm. protein,
100 gm. carbohydrate, and 2130 calories was tolerated without glycosuria. (For
details of the exercise experiments, see Chapter V.) After the fast-day of Oct.
10 another carbohydrate test was instituted with heavy exercise. Potatoes and
other high carbohydrate vegetables had to be used this time to avoid excessive
bulk. Glycosuria appeared with 210 to 220 gm. carbohydrate on Oct. 28 and 29.
Exercise was then increased, and glycosuria cleared up and did not return until
an intake of 270 gm. was reached.

On Nov. 14, the patient was discharged in apparently excellent health, free
from glycosuria and ketonuria, on a diet somewhat better balanced than before,
namely 7S gm. protein, 75 gm. carbohydrate, and 2400 calories (over 1.5 gm. pro-
tein and 50 calories per kg., reduced by weekly fast-days to 1.3 gm. protein and
43 calories per kg.).

Acidosis. — ^The fluctuations shown in the blood bicarbonate were mostly con-
nected with the exercise, experiments. The ferric chloride reaction cleared up as
stated when the carbohydrate intake reached 60 gm. on Aug. 1 without other food.
It remained absent on the fast-day of Aug. 5, but reappeared promptly with the
subsequent diet. During Aug. it became entirely negative, doubtless on account
of the low calory diet rather than the introduction of the small quantities of
carbohydrate. The subsequent occasional traces were perhaps associated with
the heavy exercise, but continued exercise produced no continuance of this reac-
tion. Alkali was not used.

Blood Sugar. — ^There is little to remark except the tendency to slight continuous
hyperglycemia. Some of the fluctuations stand in connection with the exercise
experiments. On the high diets allowed it is evident that exercise failed to
keep the blood sugar below about 0.15 per cent. This accords with other ex-
perience that it cannot be used as a substitute for caloric restriction.

Body Weight. — From 52 kg. at entrance, this was reduced to 49 kg. on Aug. 30.
Thereafter it rose as high as 52.6 kg. on Oct. 10, partly by reason of slight edema.
The carbohydrate tolerance test in Oct. produced first a sharp fall in weight due
to undernutrition, followed by a rise to 51.6 kg. due to edema. With subsidence
of the edema, the long undernutrition (29 days) of this carbohydrate test made
itself felt by a sharp drop in weight. The patient was discharged weighing 47.4
kg.; i.e., 4.2 kg. less than at the first admission.

312 CHAPTER m

Subsequent History. — ^The patient adhered to diet and exercise, and the urine
remained normal. The health seemed perfect. On Feb. 10, 1916, sugar in blood
was 0.141 per cent, in plasma 0.145 per cent, CO2 capacity 65 per cent. Weight
51 kg. On Feb. 20, the patient slightly overstepped his diet at his brother's
wedding, and brought on glycosuria which was checked by a fast-day. In Mar.
he passed through an attack of grippe and bronchitis, and showed traces of
glycosuria which required temporary reduction of diet.

Death occurred June 10, 1916. Inquiry elicited the information that there
had been an attack of acute appendicitis. On account of the diabetes the family
physician had attempted to avoid operation. Symptoms of perforation appeared
on June 5, and glycosuria had also developed. On that day the patient was rushed
to a hospital for an emergency operation. Anesthesia was given with nitrous
oxide and oxygen. Perforation of the appendix and free peritonitis were found.
Following operation he seemed to do well and became free from glycosuria. The
diet during this time was not stated. On June 9, coma was said to have devel-
oped in spite of alkali treatment and resulted in death the next day.

Remarks. — Undernutrition had the usual effect in raising tolerance, relieving
symptoms, and improving strength. The diet toward the close of the first period
in hospital was unduly high. The condition then, with sugar-free urine, rising
weight, and only a trace of ferric chloride reaction and slight hjrperglycemia, was
one ordinarily considered highly favorable in a case of this type and was clearly
superior to the results achieved by specialists who had treated this patient at
earlier and milder stages of his condition. But the return of glycosuria whUe the
patient was under favorable environment at home and adhering faithfully to
treatment was not accidental nor an indication of spontaneous downward prog-
ress, but was the inevitable result of the high diet which was producing the gain
in weight. A stUl more favorable condition was achieved during the period of
undernutrition in the first half of the second stay in hospital. The diet was then
increased to a less degree than before, and at the same time heavy exercise was
employed to use up the surplus calories and if possible buUd up the assimilation.
The effect upon both the tolerance and the general health was clearly beneficial
and no ill results were observed. Nevertheless, exercise could not entirely re-
place caloric restriction, for hyperglycemia was persistent, whereas with exercise
and a lower diet the blood sugar might have been normal. The ultimate outcome
in this type of case probably could not have been favorable on a diet as high as
that allowed. The observation upon this patient was interrupted by the im-
timely death from a cause bearing no definite relation to the diabetes. A note-
worthy point is that the patient was on liberal diet, so that he was steadUy gain-
ing weight; otherwise critics might allege that susceptibility to such an accident
was due to undernutrition. It so happens that the majority of serious infec-
tions and accidents in this series have happened to patients on high rather than to
those on low nutrition. It is possible that suitable dietetic care before and after
operation might have prevented the fatal result.

CASE RECORDS 313

CASE NO. 35.

Male, married, age 61 yrs. American; lawyer. Admitted Feb. 20, 1915.

Family History. — Mother died of typhoid at 32, father of some paralytic con-
dition at 57. Three sisters and two brothers are well; one other brother has
arthritis. A first cousin died of cancer. No other heritable disease known.
Patient has been married 34 years; wife healthy but never pregnant.

Past History. — Healthy life under excellent hygienic conditions. Grippe,
measles, whooping-cough, and mumps in childhood. Probably mild typhoid at
13. A few attacks of grippe since. No sore throats or other minor infections.
No venereal disease. Habits very regular and simple. No alcohol used until
prescribed for diabetes. No excesses in diet or indulgence in sweets. Bowels
regular. No nerve strain. Patient has been a prosperous lawyer and official in
a small New York cityunder seemingly ideal conditions of health.

Present Illness. — 11 years ago persistent backache was the first symptom.
Within a year thereafter more or less polyuria was noticed. Glycosuria was then
found, but ceased with simple abstinence from bread and potatoes. During the
ensuing year, however, glycosuria became more stubborn and 20 pounds weight
were lost. 9 years ago, on his physician's advice, the patient spent 30 days under
the care of Carl von Noorden. He received the usual treatment with green days,
oatmeal days, etc. , and was told that it was impossible for him to be free from
glycosuria. He returned with glycosuria diminished and strength increased,
with a gain of 5 pounds in weight. He adhered for 1| years to the diet pre-
scribed in Vienna, which contained liberal amounts of carbohydrate. 10 pounds
weight were lost. He then returned to Vienna for 33 days of treatment. He
again gained 5 pounds and felt better. The glycosuria was stUl present on
leaving. He again followed the prescribed diet until 1909, when he returned to
von Noorden for 31 days. This time the trouble was more persistent and there
was little improvement. The patient still carried on his regular work. In 1911
he was treated by von Noorden for 33 days with more stringent measures than
before, 2 fast-days being employed. He continued in sKghtly reduced health
until Apr., 1914, when a buU knocked him down and broke four ribs. Dangerous
acidosis came on. His medical advisor knew of the fasting treatment, and
withheld aU food for 4 days. The symptoms of impending coma passed off.
Since then he has remained subjectively in tolerable health, and came for treat-
ment only because his physician advised that the persistent glycosuria and acidosis
should be cleared up if possible.

Physical Examination. — Height 170 cm. A well developed, adequately nour-
ished, unusually rugged looking man for his age. No aCute symptoms, but a
marked odor of acetone. Mouth and throat normal. Only insignificant lymph
node enlargements. Blood pressure 120 systolic, 80 diastolic. Liver edge pal-
pable 4 cm. below costal margin in mammary Hne. Knee jerks obtained only
slightly with reinforcement. Ankle jerks sluggish. General examination is that
of an unusually healthy man.

314 CHAPTER in

Treatment.— Oa the first full days in hospital, Feb. 21 and 22, the patient re-
ceived an observation diet of 95 to 130 gm. protein, 5 to 8 gm. carbohydrate, and
1900 to 2000 calories, and excreted 25 to 22 gm. sugar, with evidently consider-
able diacetic acid. Beginning Feb. 23 he was given an 8 day fast, with 150 to
200 cc. whisky, 300 cc. soup, and 300 cc. coffee daily; no alkaU. The glycosuria
diminished, but the ferric chloride reaction became intense; the carbon dioxide ca-
pacity of the plasma remained approximately normal. The patient began to com-
plain of malaise and nausea, and appeared drowsy. On Mar. 2 he vomited. 10 gm.
sodium bicarbonate on this day failed to alter the symptoms. Therefore on Mar.
3 the fast was broken off, and a diet of 48 gm. protein, 5 gm. carbohydrate, and
1300 calories was given. This was increased on the following days, so that on
Mar. 10 the intake was 90 gm. protein, 5 gm. carbohydrate, and 2450 calories.
30 gm. sodium bicarbonate were given on Mar. 3, and the. same on Mar. 4. The
ketonuria continued heavy and the glycosuria increased, but not to anything
hke the previous figure. Mar. 12 to 16 the diet was strictly carbohydrate-free.
The symptoms which had developed on fasting had disappeared immediately on
feeding, and the patient remained entirely comfortable on carbohydrate-free
diet. Mar. 17 fasting was resumed with whisky, soup, and coffee as before.
The glycosuria promptly fell to traces. Alkali was not given. On Mar. 17 the
patient was subjectively comfortable. On Mar. 18 he complained of slight
nausea. Therefore, without waiting for absolute freedom from glycosuria, on
Mar. 19 the 630 calories of alcohol were augmented with an egg, 25 gm. bacon,
and 250 gm. thrice boiled vegetables. The clinical symptoms were thus re-
lieved, and the glycosuria also cleared up on Mar. 20, while the ferric chloride
reaction was diminished. Traces of glycosuria returned on certain of the ensuing
days. Another single fast-day withwhisky, soup, and coffee was given on Mar. 28.
The protein-fat diet was gradually buUt up, until on Apr. 2 and 3 it represented
72 to 82 gm. protein and 1750 calories, nearly half of which was alcohol. As
symptoms of danger were apparently past, it became feasible to proceed to raise
the tolerance and attack the persisting acidosis. Therefore Apr. 4 was a fast-
day with 700 calories of whisky. On the following 2 days, 10 gm. carbohydrate
were added to the whisky. On Apr. 7 whisky was diminished, and thereafter
discontinued. A routine carbohydrate test (Apr. 8 to 17) established the toler-
ance as about 100 gm. carbohydrate. At the same time the ferric chloride reac-
tion became much paler. A diet was then begun with inclusion of 15 gm. carbo-
hydrate. Traces of glycosuria were too frequent, and on May 12 to 14 the
patient fasted 3 days; nothing but 300 cc. coffee and 300 cc. soup daily was given.
Undernutrition was then continued, with persistent low diet and a routine fast-
day every week. After the fast-day of May 23, glycosuria was permanently
absent, but shght ferric chloride reactions continued. The patient was dis-
charged June 22, on a diet of 78 gm. protein, 15 gm. carbohydrate, and 2120 cal-
ories (slightly less than 1.5 gm. protein and 40 calories per kg., diminished
one-seventh by the weekly fast-days). He had become accustomed to the simple

CASE RECORDS 315

low diet, and could be depended upon to continue it accurately at home. The
general appearance was distinctly not so good as at admission; but in addition to
the altered laboratory findings, the patient insisted that he felt better and his
mind was clearer than before.

Acidosis. — ^The case illustrates the difficulties and possible danger of fasting
sometimes in long standing diabetes, when the patient perhaps appears in very
favorable condition. This patient had previously undergone fasting with benefit
after the accident with the bull. His physician considered that at that tmie the
fasting saved him from dying in coma. On the present occasion in hospital he
showed no symptoms either on mixed diet or on the change to carbohydrate-free
diet. But toward the close of an 8 day fast the typical warning symptoms de-
veloped, and were not prevented by the rather hberal use of whisky, nor relieved
by 10 gm. sodium bicarbonate. The carbon dioxide capacity of the plasma at
this time was within normal Umits and gave no warning of the critical condition,
which was recognized by cUnical symptoms alone. As usual when this condition is
taken in time, feeding cleared up the symptoms immediately. Other experience
confirms the view that the use of soda was not essential, nor was it necessary to
give carbohydrate. The mere giving of food, even though this consisted chiefly of
fat, was sufficient to reUeve the intoxication of this fasting acidosis. Also as usual
in such cases, the sensitiveness disappeared later, so that modifications of diet
were made at will without clinical disturbance. Corresponding to the normal
blood alkalinity, the ammonia nitrogen was never above 2 gm. It diminished,
but did not reach normal limits until the carbohydrate tolerance test in Apr.
The intense ferric chloride reaction was the only laboratory index which corre-
sponded to the cUnical intoxication, yet this remained equally intense when
carbohydrate-free diet had cleared up the chnical symptoms completely. This
reaction gradually faded out, but did not become permanently negative during
this period in hospital.

Blood Sugar. — The only normal blood sugar was 0.108 per cent in both whole
blood and plasma on the morning of June 14, following the preceding fast-day.
The persistent hyperglycemia was the reason for the rigorous undernutrition
period (May 11 to IS) comprising 2 days of very low diet and 3 fast-days. This
entirely failed to reduce the hyperglycemia, which was 0.2 per cent on May 15.
The treatment had been rigorous, and it was deemed advisable not to push
undernutrition further in an attempt at a rapid reduction of such a stubborn hy-
perglycemia, but rather to leave it, hke the ferric chloride reaction, to take care
of itself in the course of gradual improvement.

Weight and Nutrition. — The patient was received appearing in unusually robust
health for his age, weighing 66.4 kg. At discharge his weight was 54 kg.; i.e.,
a loss of 12.4 kg. in consequence of the' undernutrition treatment. The only
tangible sign of improvement was from the laboratory side. He claimed to feel
such benefit subjectively that he was firm in continuing treatment, but his ap-
pearance was noticeably thin and haggard, compared to that on admission. The

316 CHAPTER III

diet at discharge was sufficiently liberal that he could be expected to hold weight
or perhaps gain sHghtly.

Subsequent History. — Glycosuria remained absent, and by the end of July the
ferric chloride reaction had become negative. On Aug. 21, his local physician
(not the consultant who had sent him to the hospital) called at the Institute to
report that the patient's family and friends were worried about him, and that
although he was doing his work after a fashion, his working power and apparent
strength were not equal to what they were before treatment. Information was
otherwise obtained that the home opinion of the effect of the treatment was de-
cidedly unfavorable, and only the loyalty of the patient himself and his medical
consultant kept him strictly to the program. His local physician was assured
that a considerable period of subnormal weight and strength was unavoidable,
and the results would appear later. With continued diet and exercise the progress
continued favorable. On Oct. 13, 1915, the sugar in whole blood was 0.178 per
cent, in plasma 0.185 per cent. The weight was 57.4 kg. An increase of car-
bohydrate to 25 gm. was permitted. Steady and obvious improvement continued,
and the patient reentered the hospital Feb. 5, 1917, on request for observation,
having never shown glycosuria since discharge.

Second Admission. — ^The weight was 61.6 kg.; i.e., 7.6 kg. more than at dis-
charge, but 5.2 kg. less than at the first admission. The urine was negative for
both sugar and diacetic acid. Following the fast-day of Feb. 6, the blood sugar
on the morning of Feb. 7 was 0.115 per cent. A carbohydrate test ending Feb.
26 showed a tolerance of 240 gm. carbohydrate, as compared with the 100 gm.
in the previous Apr. Chiefly by the undernutrition in the carbohydrate test the
weight was reduced, and was 57.2 kg. at discharge on Mar. 3. The mixed diet
of Feb. 29 to Mar. 3 contained 50 gm. carbohydrate. The diet prescribed at
discharge consisted of 100 gm. protein, 35 to 40 gm. carbohydrate, and 2500
calories.

Remarks. — ^The case illustrates the feasibility and desirabiUty of effective
treatment even in long-standing cases of diabetes in advanced Ufe. Probably no
diabetic of 61 years could appear more healthy and less injured by glycosuria
than this patient, according to superficial appearances at his first admission.
There was a serious question whether it was worth while to undertake to clear up
the condition. This was done partly on advice of Dr. S. J. Meltzer, who urged
that the patient might at any time meet some accident and go into coma, or de-
velop gangrene and die from it. The known difficulties of such cases were
encountered; namely, first, the serious symptoms during fasting, and second,
the period of several months of lowered weight and impaired strength from
undernutrition. Not only, however, was relief from diabetic symptoms and the
attendant dangers ultimately achieved, but also the physical condition even at a
sUghtly reduced weight came back to a decidedly better state than before treat-
ment. The patient could think better, work better, and enjoy life more than
at any time since the first onset of his diabetes, and the objective evidences were
such that his family and neighbors were fully convinced.

CASE RECORDS 317

The primary treatment of such a case is fully as difficult as that of young
patients. In a case of this severity, halfway measures are wholly inadequate and
often injurious. The ultimate prognosis is undoubtedly better than in younger
patients. The slow improvement may be expected to continue, so that further
relaxation of diet and increase of weight may be expected. Barring accidents,
there should be no further trouble from the diabetes.

CASE NO. 36.

Male, unmarried, age 30 yrs. American; electrical engineer. Admitted Mar.
8, 1915.

Family History. — Father died of Bright's disease 5 years ago. Mother aUve,
has myxedema. Three sisters are well. One brother died of diphtheria at 4
years. Another died of diabetes at the age of IS. 13 years ago a paternal first
cousin died of diabetes at 16. No tuberculosis, cancer, syphilis, or nervous dis-
orders known in family.

Past History. — Healthy life, mostly spent in Canada, always under excellent
hygienic conditions. Measles and diphtheria in childhood. A large peritonsillar
abscess at 27 years, which lasted 2 weeks and caused fever and obstruction of
breathing.

Present Illness. — During 1913, trouble occurred with a wisdom tooth, resulting
in an abscess, and a dentist in several attempts was tmable to extract it. Thirst,
polyuria, and loss of weight were noticed shortly thereafter. In Jan., 1914, the
diagnosis of diabetes was made in Toronto. He was in hospital 10 days under
dietetic treatment, when another abscess developed about the same wisdom
tooth. This was extracted after 3 days, but necrosis of the jaw and septicemia
ensued. There was fever and delirium, and more or less infection persisted until
the end of Apr. From his normal weight of 140 pounds he declined to 90 pounds,
but during May came back to 130 pounds. At the end of May there was an
attack of acute appendicitis with pain and fever for 2 days. Another attack came
on July 28, and appendectomy was performed on July 30. There was a colon
bacillus infection of the wound, which did not heal untU Sept., 1914. Meanwhile
there were three abscesses in the neck, treated by vaccine; the last one did not
heal until Oct. The weight was now down to 115 pounds. The patient dragged
along with glycosuria and diminished weight and strength, but was not bed-fast,
until the time of admission to this hospital.

Physical Examination. — ^A well developed, moderately emaciated young man
with no urgent symptoms. Acute coryza present.- Teeth in good repair except
lower left third molar, of which only the root is present. Throat normal; no
tonsillar hypertrophy or exudate. Very slight enlargement of superficial lymph
nodes. Blood pressure 100 systolic, 60 diastolic. Reflexes normal. General
examination negative.

Treatment. — The observation diet on Mar. 9 and 10 consisted of 75 to 80 gm.
protein, 3 gm. carbohydrate, and 1670 to 2300 calories. On Mar. 10, the sugar

318 CHAPTER ni

excretion was 14.6 gm., the ammonia nitrogen 2.25 gm., and the ferric chloride
reaction intense. 4 days of fasting with whisky cleared up the glycosuria and
diminished the ferric chloride reaction and the ammonia output. Green vege-
tables were then begun, 20 gm. carbohydrate being thus added to the whisky on
Mar. IS, after which whisky was stopped. Increase of vegetables in the form of a
carbohydrate test established the tolerance as 175 gm. carbohydrate, this "quantity
being tolerated on Apr. 3, but causing slight glycosuria on Apr. 4. A mixed diet
was then rather rapidly built up, with the usual weekly fast-days. At dis-
charge on July 15 the diet consisted of 80 to 90 gm. protein, 50 gm. carbohydrate,
and 2500 calories (1.6 to 1.8 gm. protein and 50 calories per kg., diminished one-
seventh by weekly fast-days). The only special incident in hospital was the re-
moval of the root of the left lower third molar tooth on Apr. 28, after a rather
difficult half hour operation under local anesthesia. Glycosuria followed this
operation, though it will be noticed that both carbohydrate and total diet were
less than had been tolerated on former days. The slight glycosuria ceased with
a single fast-day on Apr. 29, and there was no further trouble. The patient at
discharge was not up to full normal strength, but was improved to the point
where he felt able to undertake light work.

Acidosis. — ^This was never threatening, and the carbon dioxide capacity of the
plasma remained normal. The ferric chloride reaction was not negative for any
considerable period except during the carbohydrate tolerance test. Mar. 24 to
Apr. 5. The persistence of this reaction, though slight, was one indication of the
need of more thorough treatment in a patient of this type.

Blood Sugar. — ^In conformity with the rule that glycosuria or hyperglycemia
resulting from carbohydrate alone is brief, the blood sugar on the morning of
Apr. 1 was 0.11 per cent notwithstanding the large carbohydrate ration. The
normal figure on Apr. 30, following the single extra fast-day of Apr. 29, shows how
easily hyperglycemia might have been abolished. The actual tendency of the
curve, as far as analyses were made, was progressively upward. Traces of gly-
cosuria also became more frequent toward the close. These points confirmed the
indication of the ferric chloride reactions, that the tolerance was being slightly
overtaxed.

Weight and Nutrition. — Slight undernutrition was practiced at first, then lib-
eral diets allowed, and the weight at discharge was almost exactly identical with
that at admission. The patient was over-eager for quick results. He com-
plained of hunger on slight restrictions, and found fast-days very hard. His
neurotic temperament was one excuse for the attempt to feed with a view to
maintaining the highest possible weight and strength.

Subsequent History. — Sugar remained absent and the ferric chloride reaction
slight. On July 27, an increase of carbohydrate to 60 gm. was permitted. In
Aug. the patient reported having found congenial light work, and as sugar was
still absent the carbohydrate ration was increased to 75 gm. Glycosuria remained
completely absent except for one trace in Nov. from an unintentional mistake in

CASE RECORDS 319

diet, and another in Dec. from nervousness (on the usual basis of dietary hyper-
glycemia). After Christmas, 1915, he stopped weighing food and became interested
in Christian Science. He began to add cautiously to his diet, and whenever
sugar appeared was frightened out of his trust in Christian Science and fasted
sufficiently to clear it up temporarily. In May, 1915 he began to disregard diet
and urinary tests altogether. The rapid loss of weight and strength convinced
him of his mistake, but he did not report to the Institute. He was at a mineral
water resort for a short time, and became so weak that he had to telegraph his
sister to assist him home. He arrived in New York on June 6 with indigestion,
and was obliged to fast almost completely from inability to take food, until
readmitted to the hospital on June 9.

Second Admission. — Emaciation had brought the weight down to 42.2 kg.
The patient was semistuporous, bordering on coma. Knee and Achilles jerks were
normal. June 10, the first full day in hospital, on a carbohydrate-free diet of
63.5 gm. proteia and 1450 calories, he excreted 68 gm. glucose and 4.55 gm. am-
monia nitrogen, with urinary acidity of 611 cc. n/10 (Folin). The ferric chloride
test was black, the CO2 capacity of the plasma 30.3 vol. per cent, the sugar in whole
blood 0.270 per cent and in plasma 0.385 per cent. The plasma during the entire
former period in hospital had been clear; it now appeared like cream, and showed
8.2 per cent fat. The feeding of June 9 and 10 had been employed because of the
possibility that coma symptoms had resulted from fasting. Feeding did not
clear up the symptoms. On the contrary, on June 10 the ammonia was higher
and the CO2 capacity lower than at admission the day before, and the clinical
condition appeared more critical. Accordingly, absolute fasting was begiin June
11, with nothing but 450 cc. coffee and 550 cc. clear soup daily; no alcohol and
no alkali. The fluid intake was not forced; the patient was merely encouraged to
drink rather freely, and actually took only 2500 to 2800 cc. total fluids daily. 9
days of absolute fasting diminished the lipemia to 4 per cent, the ammonia to
1.34 gm. N, the urinary acidity (Folin) to 230 cc. n/10, and the glycosuria to
5.88 gm. The CO2 capacity of the plasma rose with equal steepness to normal
limits. The hyperglycemia showed one of the peculiarities sometimes observed
in fasting; for after the sugar had gone down to 0.25 per cent in the whole blood
and 0.3 per cent in the plasma, it suddenly rose to 0.38 per cent on June 14, and
was still 0.325 per cent on June 16, though the glycosuria had greatly diminished.
All symptoms of danger had cleared up in the early days of fasting. Though the
patient was not dangerously weak, it was deemed expedient to interrupt the long
fast by a few days of low diet. Accordingly, on June 20, 35 gm. protein and 683
calories were given, and on June 21 to 23, SO gm. protein and 1000 calories daily.
The glycosuria increased, the blood sugar rose from 0.2 to 0.28 per cent, the
ammonia excretion increased slightly, and the plasma bicarbonate fell from 58.6
to 55.4 per cent. Fasting was resumed June 24 to 27, thus making 13 fast-days
in all. Glycosuria ceased, the ferric chloride reaction became negative, the am-
monia fell low, the CO2 capacity reached its highest point, and sugar in both blood

320 CHAPTER m

and plasma dropped to 0.2 per cent. The ensuing carbohydrate test revealei
a tolerance of not over 70 gm. carbohydrate in green vegetables. In this test th^
ammonia reached its lowest level. After the fast-day of July 9, mixed diet wa
begun, consisting first of 72 gm. protefn, 5 gm. carbohydrate, and 1450 calories
increased on July 24 to 85 gm. protein, 15 gm. carbohydrate, and 1700 calories
The urine was now normal, and the patient, though not so strong as at his forme
discharge, felt able to do Ught work, and was discharged on July 26 on the las
mentioned diet, with addition of 3 bran muffins and 400 gm. thrice boiled vege
tables.

Acidosis. — ^The sahent point is that both the clinical and laboratory signs o
very imminent coma were cleared up promptly and completely by fasting withoui
alcohol or alkali. Presumably alcohol would have accomplished nothing unlesi
to maintain strength. Soda might have been given if the blood alkalinity hac
not risen spontaneously. No cUnical tendency to acidosis was left behind. Th(
CO2 capacity remained fully normal. The ferric chloride reaction cleared ui
completely during the second fast and remained negative. The ammonia fel
steeply during both fasts, reached its lowest level during the carbohydrate test, anc
rose as high as 0.8 to 1.1 gm. N on the subsequent mixed diet, it being at this time
the sole indication of sUght acidosis. It is noteworthy that even though the dia-
betes was clearly worse than at the former admission and the carbohydrate in the
diet so much less, the markedly low diet as respects fat and calories now pre-
vented the excretion of diacetic acid which was almost constantly present during
the former period in hospital.

Blood Sugar. — ^The peculiarities during fasting were mentioned above. On the
carbohydrate test the fasting blood sugar remained stationary at 0.2 per cent;
the plasma sugar rose to 0.228 per cent. On mixed diet the tendency of the
blood sugar was downward, the normal value on July 24, following the fast-day
of July 23, showing that the hyperglycemia was still readily capable of control by
a low caloric diet. The sUght increase in diet at discharge brought a return oi
moderate hyperglycemia.

Body Weight. — ^The difference between loss of weight produced by underfeed-
ing for therapeutic benefit and the injurious emaciation resulting from unchecked
diabetes is exemplified.

This brief period in hospital gives an unusually striking illustration of the
possible fluctuations in water content of the tissues of diabetics, as shown by the
contour of the weight curve. As usual it fell slightly during the first days of fast-
ing. The slight rise due to edema toward the close of the fast is not uncommon,
The unique feature is the continued steep ascent on the low protein-fat diet oi
June 20 to 23. It reached 50 kg. and remained there during the 4 day fast:
i.e., a gain of 8.4 kg. in the week June 16 to 24. The edema was so intense
that there were pressure pains in the legs. It was presumably of renal (no albu-
min or casts) or obscure metabolic origin, possibly standing in some relation with
the pecuUar leap of the blood sugar, and evidently associated with chloride reten-

CASE EECOEDS 321

tion, for salt-free diet brought a fall almost as rapid as the rise. Though the
diet beginning June 10 was low, the weight rose again without visible edema.
The increase (45.7 kg. at discharge as compared with 42.2 kg. at admission)
probably represents largely water retention by tissues formerly abnormally
dried.

Undernutrition. — The following calculation can be made for 46 days of the
second hospital period (June 9 to July 25) :

46 days.

Per day
(average).

Protein in diet 1,535 .2 gm.

Nitrogen"" 245.6 "

Total nitrogen excreted 334.64 "

Nitrogen deficit (output — intake) 89 . 04 "

Total calories in diet 29,737

33.4 gm.
5.34 "
7.27 "
1.93 "
647

Subsequent History. — On Aug. 23 the patient reported that he was feeling con-
stantly better. The urine was uniformly negative for both sugar and ferric
chloride reactions. The sugar in whole blood was 0.117 per cent, in plasma
0.128 per cent, CO2 capacity 51.8 per cent. Weight 46.8 kg. An increase of S
gm. carbohydrate was permitted and tolerated. In Sept. an increase of fat, so
as to make the total calories 1830, was permitted. The weight was then 48 kg.
The patient was at work and professed himself contented with his condition and
diet. On Nov. 26, a letter was received expressing deep gratitude, and stating
that he had followed diet but wished to relieve himself of his former pledge;
though he intended to make no radical changes, he nevertheless proposed to fol-
low his own discretion. The next report received was a telegram on Feb. 2,
1917, announcing that the patient had died at 8 o'clock that day.

Remarks. — The case presents two possible etiologic factors; namely, heredity
and infection. Diets to the verge of tolerance were permitted, partly because
of the unstable temperament, but largely because their injurious effects were
not properly understood. They were fairly well borne for a munber of months
as usual, but did not serve to prevent the patient from breaking treatment.
They perhaps did more harm than the record indicates. It seems possible that
on the basis of a mild or moderate inherited tendency, active diabetes had been
developed and maintained by a series of acute infections. With the clearing up
of the infections and of diabetic symptoms there was seemingly a marked ten-
dency to improvement, as indicated by the rapidly acquired tolerance for high
diets. Possibly under sufficiently careful treatment the diabetes might to some
extent have become latent. The tendency to improvement was probably crippled
by the high diets employed. It is certain that seemingly brilliant success often
masks irreparable injury. After months or years of overdriven function a per-
manent and hopeless lowering of assimilation is found, which is blamed upon
"spontaneous downward progress." In this instance the actual disaster was
precipitated by Christian Science; but in any case with acute infectious etiology,

322 CHAPTER m

there is always the possibility that early thorough relief of dietary strain may per-
mit a degree of recovery sufficient to protect against such a misfortune.

On the second admission to the hospital the patient had learned a severe lesson
and was amenable to discipline. The results show that although his case had
become more severe, it was stiU readily controlled by radical treatment, and on
better treatment than before the laboratory findings were somewhat better,
though the weight and strength were less. After discharge the tendency to a
slow recovery of tolerance and weight was still manifest. This time New Thought
literature overcame the patient's fears, when he began to feel like himself once
more. He was of the neurotic nature predisposed to such aberrations, and they
were responsible for his death.

CASE NO. 37.

Male, unmarried, age 16 yrs. American; liigh school student. Admitted
Mar. 19, 1915.

Family History. — Mother, father, two brothers, and one sister well. No special
disease in family.

Past History. — Healthy life under excellent conditions in New York City.
Measles and chicken-pox in infancy. No venereal or other diseases. Never
used alcohol or tobacco. No excesses in diet. Up to 2 years ago his family com-
plained that he did not eat enough. Since then he has been "always ready to
eat." Has the usual appetite for candy, but has not taken naore sweets than
most boys. Never nervous or overstudious. Has been content to stand about
the middle of his class, has taken part in athletics and is now captain of the
basket-ball team of his high school. Lately he has had toothache, and just
before admission to hospital an abscess about one molar.

Present Illness.^S weeks before admission patient caught a severe cold in
connection with, a hard game of basket-ball. The following day he felt consid-
erable thirst, which he attributed to the fever accompanying the cold. Poly^
dipsia and polyuria continued, and his family noticed a lack of energy. The
symptoms progressed until, about a week ago, he was drinking water and pass-
ing urine approximately every 40 minutes. Appetite seemed to be unchanged.
He has been sleepy the past few days. The family physician, who was then
called, made an immediate diagnosis of diabetes, gave sodium bicarbonate, and
advised coming to this hospital. The patient came unaccompanied, merely for
examination. The signs of impending coma were such that he was put to bed
immediately and his family notified.

Physical Examination. — A well developed, firm muscled boy, looking perfectly
healthy except for the unnatural flush of the cheeks, noticeable dyspnea, odor of
acetone, and marked sleepiness. Tongue red and slightly coated. Teeth show
considerable caries and slight pyorrhea. Throat, congested; tonsils enlarged to
olive size. Small lymph nodes palpable in cervical, axillary, epitrochlear, and
inguinal regions. Knee and other reflexes active. Blood pressure 120 systolic,
90 diastolic. Examination otherwise negative.

CASE RECORDS 323

Treatment.— ^Ovfing to the urgent symptopis, fasting was begun immediately.
The urine from 5 p.m., the hour of admission, to 7 a.m. showed 71.3 gm. sugar and
intense ferric chloride reaction. The carbon dioxide capacity of the plasma
was 25 vol. per cent at admission. 10 gm. sodium bicarbonate and 70 cc. whisky
were given during the night. Mar. 20, the dosage was 30 gm. bicarbonate and
160 cc. whisky da,ily. By this time the threatening clinical symptoms had
passed off. Mar. 22, the bicarbonate was diminished to 10 gm., and then dis-
continued. Whisky was not used after Mar. 24. Glycosuria was absent on
Mar. 27, the ferric chloride reaction was slight, the carbon dioxide capacity of
the plasma was approxirnately normal, and the ammonia 'nitrogen, which on
Mar., 20 was 5.62 gm., had fallen to 0.73 gm. The blood sugar, which was 0.21
per cent at admission, fell steadily to 0.1 per cent on Mar. 31, On Mar. 29, 10
gm. carbohydrate in the form of green vegetables were given, and increased rather
rapidly. On Apr. 12 to 14, 175 gm. daily were assimilated, but the increase to
200 gm. carbohydrate on Apr. 15 brought slight glycosuria. After the fast-day
of Apr- 16, eggs, bacon, and vegetables were allowed on Apr. 17, representing
33 gm. protein, 15 gm. carbohydrate, and 770 calories. Slight glycosuria re-
sulted, as sometimes happens with a diet following a fast-day. This cleared up,
and higher diets were quickly tolerated with only bare traces of glycosuria. From
the latter, part of May to Aug., the diets were about 2500 calories, comprising
90 to 100 gm. protein and increasing carbohydrate up to 205 gm. On July 31,
after the fast-day on Aug. 1, another tolerance test was instituted, and in order
to give the requisite quantities of carbohydrate it was necessary to include such
foods as potatoes, corn, lima beans, peaches, and bananas. On Aug. 6, 400 gm.
carbohydrate with 83 gm. vegetable protein were assimilated. Glycosuria oc-
curred on Aug. 7 with 500 gm. carbohydrate and 118 gm. vegetable protein.
The glycosuria ceased with a green day on Aug. 8, representing 24 gm. protein
and 103 gm. carbohydrate. The patient was disniissed Aug. 11 on a diet of 100
gm. protein, 100 gm. carbohydrate, and 2450 calories. He looked and felt
entirely well and was permitted to resume school work. The only special inci-
dent in hospital was the necessary dental work to bring his mouth into good con-
dition, including the extraction of three molar teeth, which was done without
ill effects.

Acidosis.— The clearing up of the various signs of impending coma on fasting
was noted above. The carbon dioxide capacity of; the plasma fell slightly fol-
lowing the discontinuance of soda on Mar. 22, also following discontinuance of
wliisky on Mar. 24. In each case it readily rose again, and it is probable that
neither alkali nor alcohol played an essential role. The ferric chloride reactions
and the ammonia showed no such influence, On the carbohydrate test (Apr. 3
to 15) the ferric chloride reaction became entirely negative. On beginning
mixed diet, nothing was definitely altered in the CO2 capacity, and the ammonia
was only slightly higher, but ferric chloride reactions began to recur as the caloric
intake was raised, notwithstanding the fact that carbohydrate was similarly
increased. Such reactions persisted up to May 22, with 50 gm. carbohydrate in

324

CHAPTER m

the diet. Further increase to 65 gm. carbohydrate abolished them, and they
remained -absent with further increase of carbohydrate, even though fat was
also increased.

Blood Sugar. — The curve shows the characteristics of an early case, still in
the mild stage. It returned quickly to normal, rose only slightly as the diet was
built up, then became and remained continuously normal, notwithstanding the
high diet.

Weight and Nutrition. — For nearly the first month in hospital there was under-
nutrition. The practical abstinence from protein for 29 days is noteworthy,
and there must have been a large loss of body nitrogen. The weight fell during
the first part of the fast to Mar. 25, then began to rise on fasting with only 600
cc. soup and 300 cc. coffee daily, and continued to rise on green vegetables, until
on Apr. 3 it was 1.2 kg. higher than at admission and there was visible edema
of face and ankles. The weight then diminished spontaneously, but water reten-
tion evidently persisted, for the lowest point was gradually reached on May 10,
when the diet was theoretically adequate. A slow continuous gain followed,
and at discharge the weight was approximately the same as at admission.

The diet prescribed at discharge represented over 2 gm. protein and 50 cal-
ories per kg. of weight, diminished one-seventh by the weekly fast-days. Con-
sideration was taken of the fact that the patient was a growing boy; also activity
had been gradually increased, so that by July he was walking 7 miles daily in
addition to other exercise. He was encouraged to develop his muscles, avoid
mental strain, and plan a vocation in line with these purposes. In view of the
normal results of all clinical and laboratory tests, the attempt was made to let
him develop as nearly normally as possible, and the liberal diet was permitted to
this end.

Subsequent History. — The urine remained normal, and the patient kept up
with his school work and exercised by bicycling and skating. On Oct. 9, the
weight was 50 kg., it having been kept down by exercise as ordered. The physi-
cal and subjective condition was excellent, but sugar was found to be 0.232 per
cent in whole blood, 0.270 per cent in plasma. Increase of exercise was ad-
vised instead of reduction of diet. Competitive sports had been strictly for-
bidden for fear of excitement and strain. This was the only point in "which the
patient was disobedient, for he resumed basket-baU and participated in inter-
scholastic matches. More dental work was necessary, and three trips to the den-
tist were followed by slight glycosuria each time. The carbohydrate was dimin-
ished to 40 gm., and the dental operations thereafter produced no glycosuria,
illustrating the usual dietary factor. The blood sugar continued to rise, being
0.263 and 0.285 per cent in whole blood and 0.344 per cent in plasma on succes-
sive examinations. Undoubtedly exercise, by consuming surplus calories and
keeping down weight, delayed the progress of the diabetes far beyond the period
at which active symptoms would have developed at rest; but it was not able en-
tirely to take the place of caloric restriction. By request, the patient returned
to the hospital during his school holidays, after Christmas, for observation.

CASE RECORDS 325

Second Admission. — ^The weight was now 53.8 kg.; i.e., a gain of 6.2 kg. since
the first admission. There were barely perceptible sugar and ferric chloride
reactions. After 2 days of fasting a carbohydrate tolerance test was begun
on Dec. 29. Glycosuria resulted with only 175 gm. carbohydrate on Jan. 2, 1916,
and persisted when this intake was continued for 3 days. It ceased following the
green day of Jan. 5, when only 41 gm. carbohydrate were taken. Also the blood
sugar, which on Dec. 30 was 0.35 per cent, fell to 0.164 per cent on the morning
of Jan. 6. The patient was discharged on Jan. 9 and allowed to return to school,
on a diet of 100 gm. protein, 5 gm. carbohydrate, and 2100 calories (approximately
2 gm. protein and 40 calories per kg. on 52 kg. weight, diminished by the weekly
fast-days). Clinically the condition was perfect, and laboratory findings were
normal except for the hyperglycemia.

Subsequent History. — The patient did not do so well this time, showed traces of
sugar frequently and lost weight by reason of the consequent fasting. Instructions
were sent for him to return to the hospital, but he was unwilling to give up his
school work. Early in Feb. there was constipation and an attack of colicky
abdominal pain without fever or nausea, but with glycosuria. The patient hoped
to fast himself sugar-free without stopping school. He fasted 8 days, attending
school during the first 6. Glycosuria increased instead of diminishing. On Feb.
17 he was too weak to fast, and spent that and the following day lying down
at home without nausea or vomiting, with increasing dyspnea and drowsiness.
The only food eaten during the 8 days was four eggs and some bacon on Feb.
18. This seemed to give a little strength.

Third Admission. — The patient was readmitted at 3:15 p. m., Feb. 19, stupor-
ous, but intelligent when roused, with deep noisy respirations, 25 per minute;
typical odor; temperature 97.6°F., pulse. 114, small and thready; cheeks unnatur-
ally flushed and pinched; tongue dry and red; urine showing intense sugar and
ferric chloride reactions, containing enormous numbers of casts, and turning to a
solid curd of albumin with the heat-acetic test.

At admission, the CO2 capacity of the plasma was 26.4 vol. per cent. In the ab-
sence of nausea, the bowels were moved by calomel in divided doses followed by
30 cc. 50 per cent magnesium sulfate solution and a colon irrigation. Plain
fasting was imposed, with 150 cc. clear soup, and the patient was urged to drink
as much water as possible, the fluid intake on this fast-day thus amounting to
1680 cc. By the next morning the cKnical appearance was practically unchanged,
but the CO2 capacity of the plasma had fallen slightly, to 24.2 per cent. Because
of this fact, and because the acidosis symptoms were said to have come on as a
result of prolonged fasting, it was decided to feed as nearly a pure protein diet as
possible, and to give moderate doses of sodium bicarbonate such as would prob-
•ably not derange the stomach. The diet consisted of 600 cc. clear soup, 600 cc.
coffee, 300 gm. thrice boiled vegetables, steak, and white of egg, with addition of
10 gm. sodium chloride daily. The record is summarized in Table X.

326

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CASE RECORDS 327

By Feb. 21, clinical improvement was perceptible and the albumin and casts
had almost disappeared. Thereafter clinica;l betterment was rapid. The patient
was kept in bed on account of weakness until Mar. 2, after which, notwithstanding
the fasting, his strength permitted being up. The diet as shown represents first a
high and subsequently diminished protein ration, with continuous undernutrition
from the total energy standpoint. Glycosuria diminished but did not cease, and
there was a still more marked subsidence of signs of acidosis. Beginning Mar. 1
fasting was instituted, with 300 cc. clear soup, 300 cc. coffee, and 10 gm. sodium
chloride daily. The glycosuria cleared up uneventfully, also the ferric chloride
reaction became entirely negative even during the fast. The diet was subse-
quently built up gradually in the usual way, and the patient was dischargted July
29, 1916, weighing 39.6 kg., on a carbohydrate-free diet of 80 gm. protein and
1550 calories, without fast-days unless demanded by glycosuria (approximately 2
gm. protein and 39 Calories per kg.). Not only was the carbohydrate tolerance
practically nil, but the patient was now a thin semi-invalid, cheerful and able
to be about, but contrasting strongly with the fully healthy appearing lad that he
was at the former discharge. Though the urine was free from sugar and ferric
chloride reactions, and the ammonia excretion and plasma bicarbonate were within
normal limits, hyperglycemia was persistent. A bad prognosis was given.

Acidosis. — ^An example is afforded of the treatment of coma coming on during
fasting, by means of protein feeding and moderate doses of alkali. Fat would
presumably be harmful, both as furnishing acetone bodies directly and as de-
tracting from the desired undernutrition. The value of carbohydrate is question-
able with such high glycosuria, hyperglycemia, and D : N ratios. Protein presum-
ably serves to protect body nitrogen, maintain strength, and supply material for
ammonia formation, in addition to serving as a source of carbohydrate and to
promote diuresis. In this instance such treatment was successful when pro-
longed fasting, aided only with alkali, probably would have ended fatally.

Subseqiient History. — The patient remained free from glycosuria at home
except for occasional traces cleared up promptly by fast-days. At the beginning
of Sept. he developed a cold and simultaneous glycosuria. He was accordingly
readmitted to hospital Sept. 5, 1916.

Fourth Admission. — The weight was 38.2 kg. The patient was not so strong as
before, and had lost hope. No alarming symptoms were present, but a fast of
8 days was required to clear up the heavy glycosuria and ketonuria. A carbohy-
drate tolerance test with green vegetables alone showed a tolerance of 60 gm.
carbohydrate under these conditions; but no carbohydrate was tolerated with
mixed diet, and an intake of 60 gm. protein and 1200 calories was the maximum
possible without glycosuria. The patient's appearance suggested tuberculosis, but
the cold passed off readily with the clearing up of other symptoms by fasting,
and there were no later symptoms or findings on examination suggesting tuber-
culosis. The patient was discharged on Oct. 4, 1916, weighing only 35.2 kg.,
on a diet of 50 gm. protein and 1000 calories (1.4 gm. protein and 28 calories
per kg.). From the laboratory standpoint the condition was as before; i.e.,
nearly normal urine with persistent hyperglycemia.

328 CHAPTER in

Subsequent History. — The patient passed through another cold late in Nov.,
for which he was treated by a private physician who did not attempt to abolish
glycosuria and ketonuria. The cold passed ofiE, but when seen Dec. 13 the pa-
tient was in very bad condition, with edema of face and legs, and too weak to
rise from a chair without help. He was on a diet of 38 gm. protein, 10 gm. car-
bohydrate, and 1000 calories, with continuous glycosuria and ketonuria. By
Feb. 2 the strength had slightly improved, and edema was absent. He was on
a diet of 40 gm. protein, 10 gm. carbohydrate, and 1200 calories, with sodium
bicarbonate. Death occurred suddenly and without special symptoms. Mar.
29, 1917.

Remarks. — ^This was an early case of diabetes in the best type of patient, with
hereditary taint excluded as thoroughly as possible, and with the utmost intelli-
gence and fidelity in respect to everything pertaining to the treatment. The
early course was rapidly downward, threatening coma within 3 weeks, and the
case was then of the type generally described in text-books heretofore as un-
controllable. These symptoms were promptly and easily cleared up, and a
result was achieved which, according to former standards, was ideal. All cliiu-
cal and urinary symptoms were abolished and a high carbohydrate tolerance was
restored. Weight and strength were built up, and the blood sugar also was nor-
mal. The attempt was niade to let the patient return to normal activities on a
liberal caloric ration. The activity may have been permissible. The diet was
calamitous. It is not to be supposed that the carbohydrate allowance was too
high. There is not necessarily any harm in the fact that the protein at the
first discharge was up to the Voit standard (1.7 gm. per kg.; one-sixth of total
calories). But the average energy intake was 43 calories per kg. Vigorous
exercise and moderate restriction of weight did not atone for this overload im-
posed upon a weakened metaboUsm. Efl&ciency and health are known to be pos-
sible on a far lower intake. With some reduction of weight, Ufe could have been
well maintained on half to two-thirds this number of total calories. As usual,
the time actually arrived later when the boy was compelled to live on less than half
this number of calories. The fatal mistake lay in imposing this strain upon his
weakened function at the outset, so that it later broke down and was incap-
able of carrying adequately half this burden. The proper treatment would clearly
have consisted in limiting the burden in the first place, so as to avoid such a break-
down. The case is a perfect example of what was formerly called "spontaneous
downward progress" in diabetes.

By comparison with other cases taken under far worse conditions and treated
on a different principle, it can be concluded that the downward progress in this
case was due chiefly or solely to the treatment employed. Even in the later stages
the diets permitted were such as taxed the weakened tolerance to the utmost.
But the essential harm was done at the most favorable period, and the fatal out-
come was assured by the methods employed at the very time when the prognosis
seemed brightest.

CASE RECORDS 329

CASE NO. 38.

Female, married, age 39 yrs. Russian Jew; housewife. Admitted Mar. 20,
1915.

Family History.— FaXhex died at 65. Mother, one brother and sister are well;
one brother died of phthisis. No other diseases known.

Past History.— No illnesses known. Said to have been treated at a hospital
2 years ago for "large liver and abdomen," cured by wearing a support. Habits,
appetite, and bowel action normal. No excesses. Last menstruation was S
months and 3 weeks before admission.

Present Illness. — Began with chilly sensations and malaise 1 week ago,
followed by cough, fever, and pain, particularly in left lower chest.

Physical Examination.— A well developed and nourished woman, 5 or 6 months
pregnant; flushed cheeks, slightly bluish lips; lymg in bed breathing about 40
times per minute and groaning frequently. Tongue coated and dry; teeth false;
tonsils and lymph nodes not enlarged. Pulse 110, temperature 102.8°. Blood
pressure 150 systolic, 90 diastolic. Signs of pneumonia of left lower lobe. Liver
edge 3 cm. below costal margin. Knee jerks not obtainable. Examination
otherwise negative. Sputum was mucopurulent, yellowish gray, containing
Gram-positive diplococci, not agglutinated by Pneumonia Serum I or II. Blood
culture was sterile. Leucocytes 22,000, polymorphonuclears 91 per cent, lympho-
cytes 5 per cent, large mononuclears 4 per cent. Urine contained some albumin
and casts and showed heavy sugar and ferric chloride reactions.

Treatment. — The patient was received on the pneumonia service, and the finding
of diabetes was unexpected. The temperature feU to normal within 24 hours,
but the pulse and respiration continued elevated.

After death a needle inserted in the third intercostal space close to the ster-
num, with the idea of obtaining blood from the heart, yielded an abundance of
very turbid gray fluid, which clotted quickly on standing, showed leucocytes
but no bacteria in films, and was sterUe on culture — apparently a large peri-
cardial effusion. Necropsy was not permitted.

Remarks. — ^This is another example of diabetes discovered during the course
of an acute infection. Whether the infection produced it, or (more probably)
made active a latent or mild diabetes, is undetermined. The severity of the
acidosis is indicated by the low blood bicarbonate with large doses of alkali.
In expectation of the use of such doses, cathartics were omitted, and, as antici-
pated, moderate persistent diarrhea was kept up by the bicarbonate, the dis-
crepancy between fluid intake and output being thus accounted for. The impres-
sion was created that the alkali in such doses was definitely beneficial, and that
smaller doses would not have sufficed. Notwithstanding the combination of in-
fection and existing coma on Mar. 26, the acidosis symptoms passed off, and the
blood bicarbonate on the day of death was nearly normal. It is possible that
death was partly due to the diabetic intoxication, which may exist in the absence
of some of the signs of acidosis, but there is entirely sufficient cause for death

330

CHAPTER III

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332 CHAPTER III

without this assumption. It was not the intoxication sometimes attending upon
fasting, because the typical nausea was absent, and the food retained on Mar. 29
.brought no improvement. In summary, it may be said that pneumonia, middle
ear infection, death of fetus with subsequent artificial delivery, and either peri-
carditis or empyema, constituted a sufficient explanation of the fatal result,
and under these conditions 5 days of very low diet followed by 5 days of fasting
failed to control the diabetes.

CASE NO. 39.

Female, unmarried, age 27 yrs. American; teacher. Admitted Apr. 3,
1915.

Family History. — ^A maternal grandfather died of cancer with suspicion of
accompanying diabetes. A paternal aunt was insane 15 years ago, but has ap-
parently recovered. Patient's mother died of diabetes at 37. Father is well,
aged 70, but had nervous breakdown 25 years ago which kept him from work
for 3 years. Strong neurotic element in family. A brother of patient is a young
physician, of nervous temperament. A sister died of heart trouble within a
few months after birth. No syphilis, tuberculosis, or other diseases known.

Past History. — General healthy life under good hygienic conditions in small
New England towns. Several childhood diseases, including scarlet fever, said to
have been followed by ear trouble and nephritis. No other illnesses. Habits
regular; always nervous in disposition.

Present Illness. — ^About 4^ years ago headaches began and transitory poly-
dipsia and polyuria. The patient was first dieted by a local physician, then be-
ginning in the spring of 1913 she was under Dr. Jbslin's care several times. He
found her a model patient in hospital and the glycosuria was easy to stop, but
the patient appeared mentally incompetent whenever she returned home and
never had the will power to adhere to diet. On certain occasions she
wandered from home in lapses of consciousness, and she was regarded by Dr.
Joslin as definitely insane, though bright and active most of the time. In
the summer of 1914, after heavy mental and physical strain, she suddenly lost
consciousness for 1 day and was stuporous for 6 days thereafter. Her local
physician called the condition diabetic coma. She recovered on fasting and
bicarbonate. Thereafter she made some attempts to follow diet, but home con-
ditions were difficult and glycosuria and ketonuria were continuous.

She was admitted to a New York hospital in Mar., 1915, with facial neuralgia
of intense type. Here again glycosuria cleared up rather easily, but there was
the same difficulty regarding adherence to diet, and here also the patient was
considered mentally irresponsible to the point of insanity. The neuralgia, how-
ever, ceased with the improvement in the urinary symptoms. The patient was
financially unable to remain longer under hospital expense, and was admitted
to this Institute on Apr. 3, 1915, for the purpose of testing the effects of pro-
longed thorough treatment, not only upon the diabetes but also upon the nervous
and mental condition.

CASE RECORDS 333

Physical Examination.— Yiti^t 168.1 cm. A well developed and nourished,
nervous appearing young woman. Hair thin, short, and dry. Eyes slightly
prominent. Suspicion of slightly enlarged thyroid on palpation. Knee and
ankle jerks normal. Examination otherwise negative.

Treatment. — Glycosuria and ketonuria were present. After a single fast-day
on Apr. 4, notwithstanding faint traces of glycosuria, small quantities of green
vegetables were begun. Glycosuria stopped even while they were increased, and
remained absent until, on Apr. 15, the vegetable diet (including com and peas)
represented 42 gm. protein and 150 gm. carbohydrate. Although the fat in such
diets was only 40 gm., marked ferric chloride reactions steadily persisted with
this carbohydrate intake, and with 170 gm. carbohydrate on Apr. 16. Apr. 17
was a fast-day followed by diets of 800 and 450 calories on Apr. 18 and 19, and then
6 days of complete fasting, 150 cc. clear soup being permitted, except on Apr.
23 and 24, when nothing but water was given. The persistent glycosuria and
elevated blood sugar strongly suggest surreptitious eating during this time.
The usual diet was begun on Apr. 26 and rapidly increased, until for a short time
after May 24, 90 to 100 gm. protein, 40 gm. carbohydrate, and 2300 calories
were tolerated. On account of persistent slight glycosuria (June 3 to 7) fasting
was imposed. No other interpretation seems possible than that this was due to
forbidden food obtained in some manner not discovered; but the policy of fast-
ing until glycosuria ceased was a salutary check to such practices. Thereafter a
slightly lower diet was tolerated with occasional traces of glycosuria, some of
which were confessedly, and others probably, due to candy or other prohibited
foods. After fast-days on July 24 and 25, a carbohydrate test was instituted, and
showed a tolerance of approximately 300 gm. carbohydrate ip the form of green
vegetables. The hospital discipline had benefited the patient, and this indica-
tion of improvement was a great encouragement to her.

She was discharged Aug. 13 on a diet of 100 gm. protein, 30 gm. carbohydrate,
and 1900 calories (about 1.8 gm. protein and 34 calories per kg.), the weekly
fast-days reducing the average to about 1.4 gm. protein and 30 calories per kg.
She promised faithfully to adhere to this diet. There was unmistakable psychic
as well as physical change in the patient, and though still nervous she was clearly
more dependable and better fitted to take care of herself.

Acidosis. — At entrance the ammonia nitrogen was only 0.56 gm. and the
ferric chloride reaction mostly no more than moderate; but the plasma bicarbonate
showed the rather low level of 47 per cent on Apr. 5 and 45 per cent on Apr. 7. It
thus fell slightly during the days of very low carbohydrate, which were almost equiv-
alent to fast-days (10 gm. carbohydrate and 300 cc. soup daily). With continu-
ance of undernutrition and slight increase of carbohydrate, it rose sharply within
normal limits by Apr. 9, without the use of alkali. Thereafter the curve ran a
normal course but seemed to tend to fall with fasting, being found slightly below
normal on May 3, following the preceding fast-day, and again after fasting on
July 26. The consistent course of the ammonia curve was low. A slight ferric

334 CHAPTER in

chloride reaction tended to persist. It gradually faded out and became negative
in periods, and after the carbohydrate test in July and Aug. it became consistently
negative.

Blood Sugar.— On Apr. 7, just as the glycosuria was clearing, the blood sugar
was just below 0.2 per cent, indicating a normal renal threshold. With further
days of low carbohydrate, it had fallen to normal on Apr. 9. The carbohydrate
tolerance test led to hyperglycemia of 0.22 per cent with glycosuria on Apr. 16.
The excessively high figure shown on Apr. 22 was not checked and therefore
might have been a mistake. Thereafter the values tended to fall below 0.15
per cent. Other work made it necessary to stop the analyses; on this case after
May 18. >

, Weight and. Nutrition. — The patient entered in a very well nourished condition
weighing 59.2 kg. She was still well nourished at discharge, weighing 55.8 kg.
The net result of treatment was thus undernutrition to the extent of a loss of 3.4
kg. With the clearing of diabetic symptoms there W9,s the usual gain in strength
and well-being, and the patient felt entirely well at discharge.

Subsequent History.— The: patient resumed her regular work at home and fol-
lowed diet surprisingly well. On three occasions she went' on what she termed
"sprees" of carbohydrate, but experienced symptoms of weakness and.mp,laise
within a limited number of hours after the onset of the heavy glycosuria, and
cleared up her condition, generally after some delay, by fasting, on one or two
occasions as long as 5 days. Against external as well as internal difficulties she
kept up a continuous effort to remain sugar-free, and notwithstanding the lapses
from diet, continued to gain in weight and subjective health. On account pf
sugar and ferric chloride reactions in urine specimens received, it became advis-
able to readmit the patient on Jan. 12, 1916, 5 months after discharge.

Second Admission. — The weight had now risen to 64.1 kg.; i.e., 4.9 kg. more
than at the former admission, and both the physical and mental condition ap-
peared excellent. On the diet prescribed at discharge, the plasma sugar was
0.264 per cent and the CO2 capacity 49 per cent. There was a heavy ferric
chloride reaction, and 2.18 gm. ammonia nitrogen in the > urine. Fast-days on
Jan. 19 to 20 sufficed to clear up the glycosuria, but the tolerance on the ensuing
days with green vegetables proved to be now only 50 gm. carbohydrate. Though
diets lower in both carbohydrate and total calories were employed, it was diffi-
cult to obtain freedom from traces of glycosuria. During late Mar. and early .
Apr. there was decided intolerance for a diet of 65 gm. protein, 15 gm. carbohy-
drate, and 1500, calories. After Apr. 16, carlaohydrate was excluded. Even on
diets as low as 60 gm. protein and 1000 calories, traces of glycosuria recurred.
But with continuance of this undernutrition they remained absent after May
2, and by May 12, 70 gm. protein and 1400 calories were tolerated. With redu,Cj-
tion of one-seventh by weekly fast-days, this represented approximately 1 gm.
protein and 20 calories per kg. of weight. The patient was discharged on this
diet May 13, 1916. , ,

CASE RECORDS 335

Acidosis. — The CO2 capacity of the plasma rose easily within normal limits
without the aid of alkali, and remained so except for a single low reading on
May 9. The ammonia excretion at the outset was much higher than before,
i. e. 2.18 gm. N; also the ferric chloride reaction was heavier. Thus these signs
indicated a higher acidosis than at the former admission, though the plasma
bicarbonate was 2 per cent higher than then. Isolated determinations on Feb.
7 and 21 indicated about the same subsequent level of ammonia as at the pre-
vious period in hospital. The ferric chloride reaction cleared up much more
easily and promptly than before, although the diets were so much poorer in
carbohydrate than before and frequently carbohydrate-free. This result is ex-
plained by two causes, first, the previous treatment, and, second, the lower total
caloric i value of the diets at this admission. The ferric chloride reaction was
thus negative on carbohydrate-free diet at discharge.

Blood Sugar. — An aggravation of the condition was indicated by the fact that
even on low diets the blood sugar never became normal, but remained above,
rather than below 0.15 per cent. More rigorous treatment could presumably
have reduced the hyperglycemia even at this stage.

Weight and Nutrition. — The patient's gain in weight during her absence from
hospital would once have been regarded as an improvement. Its real meaning
is that the diabetes was sufficiently mild to permit a gain in weight even in the
presence of glycosuria, and in this mUd stage injury was wrought by exceeding
the true functional power with respect to both diet and weight. After readmis-
sion to hospital, the weight at first fell from undernutrition, then fluctuated,
and on two occasions, namely Mar. 7 and 8, and Apr. 28, rose higher than at ad-
mission, because of marked edema. This edema was not associated with any alkali
administration, but may have been due to sodium chloride. The weight at dis-
charge was 61.2 kg., being 2 kg. higher than at the first admission and 2.9 kg.
lower than at the second admission. A portion of this weight may stUl have
been abnormally retained water, which however was not apparent on examina-
tion. The diets in general represented undernutrition, and the diet at discharge
meant further undernutrition and reduction of weight.

Subsequent , History. — The patient undertook to support herself by visiting
and other duties in connection with diabetic patients of a physician in New
York, and one stay at a country place was also arranged. She remained free
from glycosuria through the summer, but her diet became uncertain by reason of
her preparing her own meals under irregular conditions and making trials of
various modifications to suit herself. She finally undertook too heavy a load of
work and took too high diets in the attempt to keep up with her ambitions.
She managed to remain in fair condition as respects, diabetes, and in good con-
dition as respects general health, until readmitted Dec. 30, 1916.
■ Third Admission.— The weight was still 62.7 kg., partly due to edema. The
general appearance, strength, and behavior showed no perceptible change.
Downward progress was indicated by the fact that a 7 day fast was neces-

336 CHAPTER in

sary this time to bring the glycosuria under control. The subsequent history in
hospital was uneventful. The patient broke diet on a few occasions, otherwise
she was maintained sugar-free, and was dismissed Apr. 10, 1917, weighting 57.2
kg. on a diet of 60 gm. protein, 2.5 gm. carbohydrate, and 1300 calories. The
patient's intentions in regard to work were now the principal difSculty. She
was determined to carry a heavy load of work, and was not willing to undergo
undernutrition to a point which would diminish her working capacity. As
inevitable in such cases, the long abuse of the weakened assimilative power had
now brought the point where maintenance of full weight and working power was
impossible. The tolerance could be benefited only by undernutrition diets such
as prescribed. Such reduction must continue for several months before any gain
could be expected, and the damage already wrought -was such that a full return
to the former tolerance was undoubtedly impossible. The patient, though intelli-
gent and grateful, was unwilling to accept life on these terms, and proposed from
her knowledge of diets to nourish herself with a view to temporary working
capacity as long as possible.

Subsequent History. — The patient took mixed diet with restriction of all three
classes of food, but the period of ability to work was very brief. All her former
symptoms quickly returned except the neuralgia. The mental abnormality
again showed itself markedly. Though appearing bright and merely nervous in
public, in private she tore her clothing, bit and otherwise injured herself, and
made several attempts at suicide. She recognized symptoms of acidosis,
and accordingly excluded fat almost completely from her diet. It was learned
indirectly that she was in serious condition, and she was accordingly sent for
and brought back to the hospital by a nurse on June 18, 1917.

Fourth Admission. — There was a history of edema a week before. The pa-
tient took two capsules of 8 grains diuretin, and edema is said to have disap-
peared rapidly, and epigastric pain began. Smce then weakness and dyspnea
have rapidly increased, so that she has remained lying down for the past 2 days.
On the day before admission there was nausea and vomiting, and she took two
teaspoonfuls of sodium bicarbonate; otherwise she has had no alkali. Also dur-
ing these 2 days she claims to have fasted, partly from lack of appetite and
partly in the attempt to treat herself for acidosis. Weight was 58.1 kg.; i.e.,
1.1 kg. less than at first admission. The patient lay in bed, evidently extremely
weak. The general appearance was about as before. Neither emaciation nor
edema was present, also the tissues were not perceptibly dry or flabby. There
was a deep dusky flush of cheeks, involving lower eyelids. Air-hunger was in-
tense; deep pauseless respirations 22 to 23 per minute as the patient lay
in bed; so extreme on the slightest exertion that drinking and speaking were
difficult. The patient dozed continually when undisturbed, but roused easily and
rather nervously. Intelligence was fully clear, and she was entirely cheerful,
while convinced that death was imminent. Physical examination was negative
except for a row of herpes vesicles beginning to dry up under the left breast.

CASE RECORDS 337

These and associated tenderness explained the epigastric pain still complained
of, as due to intercostal neuralgia.

Inasmuch as symptoms of serious acidosis had begun and persisted while fat
was diminished or even excluded from the diet, and signs of coma had appeared
after 2 days of supposedly complete fasting, it was difficult to decide upon a line
of treatment for the threatening crisis. It was feared that the existing nausea
would be increased by alkali. An attempt was therefore made first with plain
fasting with soup and coffee and water forced to the limit of capacity. The
plasma bicarbonate was 30.5 per cent, the heart and kidneys were keeping up well,
and there was no sign of immediate death. It therefore seemed most conserva-
tive to wait a few hours to learn the behavior under fasting alone. The actual
progress was rapidly downward, perhaps partly on account of exhaustion from
the trip to the hospital. Unmistakable progress into coma was evident. The
patient was received at 4:30 p.m. By evening moderate doses of alkali by
mouth were begun; by midnight there had been given 10 gm. sodium bicarbonate,
30 cc. whisky, and 2105 cc. total fluids. By 9 a.m. June 19, an additional 15 gm.
sodium bicarbonate and 30 cc. whisky had been taken, yet the plasma CO2 had
fallen to 20.7 per cent, and the sugar and total acetone of the plasma were de-
cidedly increased. During June 19, 1 gm. doses of sodium bicarbonate were
given hourly with 5 gm. doses of calcium carbonate, in the hope that the latter
would help settle the stomach and possibly have some acid-neutralizing power.
Whisky was given in 15 cc. doses every 4 hours, 1800 cc. soup during the day,
and 15 gm. sodium bicarbonate. The total fluid intake was 9805 cc. By 10:30
p.m. improvement seemed to have been obtained. The breathing seemed
quieter, the consciousness clearer, and the CO2 capacity had risen to 27.7 per
cent. By the next morning the patient had begun to refuse bicarbonate because
of nausea, and the coma sjonptoms showed increase. An attempt was therefore
made to supply fluid and a moderate quantity of alkali intravenously. Accord-
ingly, 500 cc. physiological saline solution, containing 13 gm. sodium bicarbonate
were given slowly through a needle. The breathing became quieter, but an
attack of vomiting resulted and consciousness did not improve. It was then
attempted to feed protein in the form of white of egg mixed in the soup. The
small quantities thus given were retained several hours, then vomited. Com-
plete unconsciousness came on, with continuance of the intense dyspnea, and
nothing seemed left but to attempt to raise the blood alkalinity by larger doses of
soda intravenously, notwithstanding the known danger. Accordingly 1 hter of
saline solution containing 38 gm. sodium bicarbonate was given in an injection
into the arm vein in half an hour. Dyspnea diminished. The pulse, which was
strong, was unchanged. The flush of the cheeks became paler. Consciousness
was not restored, and an attack of vomiting was excited. Unconsciousness with
slight restlessness continued until 5 p.m., when there occurred the sudden death
without warning which is rather characteristic following large intravenous doses
of alkali. The principal data are contained in Table XII.

n

a

d
o
p

9:00 a.m.
12:00 n.
10:30 p.m.

9:00 a.m.
2:00 p.m.
Autopsy:

•ODOOI
«d3nO}3Dl!I^OX

i

1^

105.0

116.0

93.0

112.5
146.5
176.4

■M 001
Bd (3no;33B
s^) 3ii^nqXxo-g/

s

1

M 1 ■

91.0
108.0

•DD GOT "<! 3B"

t

1

1 1 1

55.5
68.4

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ON 0\

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1—1

2

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338

CASE RECORDS 339

Remarks.— This was one of the cases with exaggerated protein catabolism, as
indicated by the nitrogen excretion of 23.7 gm. on June 19. On June 20, an equal
or higher quantity must have been eliminated, but large quantities of urine passed
involuntarily were lost, and also death occurred at the end of 17 hours of this
day. Any error of diet as an explanation of the high D : N ratios is excluded,
as the patient was stuporous and isolated in a room with a special nurse. Only 2
days of fasting, according to the patient's report, had intervened since her period
of liberal diet, including carbohydrate. The nutrition was well maintained as
stated, and it must be assumed that with the rapid and intense change for the
worse, body glycogen was being swept out.

Several lines of treatment are open in such a case, but death occurs in a great
majority under these circumstances no matter what is done. Treatment without
alkali and -vjithout food, but supplying fluid and salt, was first tried with ominous
results. Another possibility would have been fasting with alkali from the outset.
Dosage by mouth could have accomplished nothing more by reason of nausea.
There might have been some real helpfulness in small intravenous doses of bicar-
bonate at intervals of a few hours, perhaps alternating with doses by mouth.
It appeared, however, that considerable quantities of alkali were necessary to
affect the blood alkalinity, and this excited nausea even when given intravenously.
Another possibility lay in feeding with or without alkali. It is highly question-
able if carbohydrate is of any benefit in the presence of a maximal D : N ratio.
Fat would seem to promise nothing but harm. Protein might have been bene-
ficial; but again it may be that an attempt to feed anything wiU sometimes aggra-
vate a condition of impending coma. A noteworthy feature is the fact that the
renal function was weU maintained to the end, and large quantities of urine were
passed involuntarily in the closing hours of life. It is now less common for pa-
tients received with impending coma to go into coma under treatment, but with
the exaggerated protein catabolism and continued maximal D : N ratios, such a
result is still often unavoidable.

In its general aspects the case illustrates the interrelation of diabetes and
nervous disorder, and the actual symptomatic improvement of the latter under
careful treatment of the former. Had either the psychic state or the environ-
ment been more favorable, something might have been accomplished; but with
both adverse, the patient made a brave effort but lost in the end.

CASE NO. 40.

Male, unmarried, age 29 yrs. American; doorman. Admitted Apr. 12,
1915.

Family History. — Little known; no history of disease obtainable.

Past History. — Measles, whooping-cough, scarlet fever in childhood. Right-
sided pneumonia 15 years ago. Neisser infection, also chancre some years ago;
no secondary symptoins and no treatment. Frequent colds, but rarely sore

340 CHAPTER III

throat. Formerly used whisky to excess, but recent alcoholism denied. He
smokes pipe and cigars in moderation, and takes two cups of coffee and three
of tea a day. He sleeps well, has poor appetite, and regular bowels. No known
loss of weight or other diabetic sjrmptoms.

Present Illness. — Patient entered on the pneumonia service 24 hours after
initial chill. He had a severe Type I pneumonia involving lower lobes on both
sides, with positive blood culture. Leucocytes 24,800, polymorphonuclear 90
per cent. Highest temperature 104°. Blood pressure 125 systolic, 70 diastolic.
Physical examination otherwise negative.

Treatment. — Urine was smoky red and showed heavy albumin, slight Benedict,
and moderate ferric chloride reaction. He was treated on the pneumonia serv-
ice with Type I pneumococcus serum. The blood became promptly sterile;
the temperature, pulse, and respiration remained elevated. On Apr. 12, the diet
consisted of 370 cc. milk, 150 cc. broth, and 150 cc. albumin water. On Apr. 13,
300 cc. albumin water, ISO cc. soup, and ISO cc. cocoa were given, and there
was shght glycosuria and a slight ferric chloride reaction. On Apr. 14, 700 cc.
albumin water and ISO cc. soup were the diet, and both sugar and ferric chloride
reactions diminished to traces. Apr. 15 and 16, the diet was similar but included
also 200 to 400 cc. mUk. Traces of sugar and diacetic acid persisted. Meanwhile
the temperature ranged from 101. 2-103. 6°F. Beginning Apr. 17, the patient
was placed partly under the care of the diabetic service because of abnormal
drowsiness and hyperpnea. On that day 15 gm. sodium bicarbonate were given,
and the diet was changed to clear soup and whisky. On Apr. 18, 40 gm. sodium
bicarbonate were given, and the previously acid urine turned neutral for part
of the day. On Apr. 19 another 40 gm. sodium bicarbonate were given, and the
urine was neutral throughout the day. On Apr. 20, the urine again turned acid,
but another 40 gm. bicarbonate then turned it alkaline. Continuance of 40 gm.
sodium bicarbonate on Apr. 21 and 30 gm. on Apr. 22 kept the urine neutral
or alkaline. Meantime the ferric chloride reaction, from almost negative, had
became intense. Under the influence of the alkali dosage the drowsiness cleared
up. Apr. 23, 50 gm. carbohydrate in the form of. green peas were tolerated, but
100 gm. in the form of peas and potatoes on Apr. 24 caused slight glycosuria.
Beginning Apr. 25 a diet of soup, eggs, and vegetables was given, mostly about
1000 calories. Because of the stubborn ferric chloride reaction, fastmg was im-
posed on May 2 and 3, and then a diet of vegetables up to May 6, containing a
maximum of 75 gm. carbohdyrate. On May 7, a low carbohydrate-free diet of
less than 500 calories was given for the purpose of avoiding too long continued
abstinence from soUd food in a patient with infection. A mixed diet was then
gradually built up, glycosuria appearing on May 16 with an intake of 67 gm. pro-
tein, 75 gm. carbohydrate, and 1700 calories. The diet nevertheless was still
built up, and the tolerance rapidly improved with subsidence of the infection.
The signs in the lungs persisted unduly long. Sermn sickness with urticarial
eruption was present Apr. 20 to 26. On May 10, the left seventh rib was resected

CASE RECORDS 341

under local anesthesia for drainage of the empyema. It will be noted that gly-
cosuria and a trace of ferric chloride reaction appeared on May 11, seemingly in
consequence of this operation, and promptly cleared up without reduction in
diet. The temperature subsided somewhat, but persisted in the neighborhood
of 100°. Albuminuria had gradually diminished and was negative after May 10,
but edema of the ankles persisted. On June 12, there appeared a fusiform swell-
ing of three fingers of the right hand, and later also in joints elsewhere. The tem-
perature rose at this time, but there was no glycosuria, and the ketonuria was
only such as could be explained by the high fat of the diet. Thereafter the
temperature gradually diminished and was normal after July 1. From the
diabetic standpoint, the diet was built up to a high level, not only for the pur-
pose of strengthening the patient, but also for the purpose of testing his toler-
ance. The latter proved to be almost unlimited. Carbohydrate was increased
through the various classes of food, until the tolerance was found above 200
gm. in diets containing fruits, potatoes, cereals, and bread. _ Cane sugar was
then permitted, beginning with 50 gm. on July 19, and glycosuria remained
absent until a brief trace appeared on July 23 on an intake of 119 gm. protein,
380 gm. carbohydrate, and over 3900 calories. On July 22, he had tolerated such
a diet, including 200 gm. cane sugar distributed throughout the day. On July
23, the carbohydrate allowance included this same quantity of sugar, but it was
given all at once, and a trace of glycosuria was present for a few hours. The
patient was therefore sent out on fuU mixed diet, on the presumption that the
diabetes had been transitory.

Acidosis. — ^The case is an illustration of threatened coma under the influence
of infection in a patient never known to have been diabetic, kept on very low
diet because of the inability to take more, and with only slight sugar and ferric
chloride reactions in the urine. The actual acidosis was revealed by the quanti-
ties of alkali required to turn the reaction of the urine, and by the intense ferric
chloride reactions which resulted. Relatively few analyses had been made at the
outset while the infectious features predominated. On Apr. 21, the first am-
monia determination showed the low value of 0.59 gm. N under the influence of
alkali. With omission of alkali, the ferric chloride reaction cleared up quickly
but temporarily, and the ammonia nitrogen on Apr. 24 shot up suddenly to nearly
2.5 gm. By Apr. 26, adjustment had occurred under the influence of continued
undernutrition and a little carbohydrate, and ammonia values thereafter never
reached an alarming level. More or less ferric chloride reactions recurred until
June 16, especially by reason of the high fat intake, but thereafter 75 gm. or more
of carbohydrate in the diet sufficed to abolish ketonuria even with abundance
of fat.

Weight and Nutrition. — The 1st month in hospital represented marked under-
nutrition, particularly in view of the fever. The body weight was kept up by
edema. Beginning May 7, there was a sharp decline in weight with subsidence
of edema, and after June 4 the weight rose rather rapidly under the liberal diets.

342 CHAPTER III

Remarks. — The case is an example of diabetes occurring with an acute infection
under circumstances which make it appear that the infection had given rise to
the diabetes. It is open to speculation whether the diabetes would have
passed off if heavy glycosuria had been maintained by excessive carbohy-
drate feeding from the outset, especially as this might actually have been em-
ployed under former methods of treatment for the purpose of controlling acidosis.
It was also important to determine whether the diabetes was actually transitory,
presumably the result of direct or indirect involvement of the pancreas, or whether
the infection merely brought into prominence a latent diabetes. The normal
sugar tolerance at discharge would point to a genuinely transitory diabetes.
On the other hand, the only decisive test would lie in following such a patient for
many years. If diabetes ultimately became manifest, it might then mean either
a latent diabetes, antedating an infection and temporarily made active by it, or it
might represent injury of a previously normal pancreas by the infection, with tem-
porary recovery to a considerable degree, with impairment and later breakdown of
the internal function. None of these questions could be answered because the
patient was lost sight of in spite of attempts to foUow him up. •

Among the features of the treatment, the most striking seems to be a defi-
nitely beneficial effect of alkali which cleared up symptoms threatening coma,
when fasting and low diet were accompanied by dangerous acidosis and when the
patient was in no condition to take much food. It is also worth noting that
coma may threaten under such conditions with only sUght sugar and ferric
chloride reactions and with diabetes apparently of mild degree.

CASE NO. 41.

Male, married, age 52 yrs. Irish; poKtician. Admitted Apr. 23, 1915.

Family History. — Parents died in old age. One brother well; two died in in-
fancy. One sister well; one died in infancy; one died of tuberculosis at 33. There
was mental disorder running through several generations on the mother's side.
Two of the patient's aunts died in insane asylums. No diabetes or other diseases
in family.

Past History.— Healthy and checkered life. Measles, mumps, chicken-pox,
scarlet fever, diphtheria in childhood; no sequelae. Bom in Ireland, ran awaly
to sea at age of 20, and worked mostly as a stoker in the tropics for 7 years, but
continued to enjoy good health. He then came to New York, worked at manual
labor for a number of years, then gained influence in labor organizations and poU-
tics, and has since been occupied in ofiicial positions. There was cough and
loss of weight shortly after his arrival in New York; tuberculosis was diagnosed, .
but there was apparently complete recovery. He also had pleurisy and "shingles"
20 years ago, but recovered rapidly, and has never been iU since. Venereal his-
tory consists in Neisser infection in 1883, followed by inguinal buboes treated by
incision in hospital. Chancre in 1885, followed by slight rash 3 weeks later.

CASE RECOIIDS 343

Habits have generally been good in view of hard life. Not mbre than 2 or 3
drinks a day, generally beer. Has never used tobacco. The diet on shipboard
left him with more or less indigestion. Bowels usually regular. He has eaten
rather liberally of sweet foods.

Present Illness. — 4 years ago he was troubled with dry throat following a
cold. Physician in routine examination found 2 per cent glycosuria. Shortly
after this polyphagia, polydipsia, and polyuria set in, but disappeared on mod-
erate restrictions of diet. There has been no attempt to make him sugar-free.
6 months age he barked his shins; these were very slow in healing, and collections
of pus required opening. Since Mar. 17, he has had a grippe infection and con-
siderable impairment of general health, and his physician advised him to come
to the Institute for diabetic treatment. The loss of weight has amounted to 15
pounds in the past 3 years.

Physical Examination. — Height 172 cm. Awell developed, strong looking, some-
what obese man, showing no distress, but with cyanosis of face. Temperature 1 02°
F., pulse 120, respiration in bed 36. Breathing not of air-hunger type. Teeth all
false. Throat slightly congested; tonsUs show slight hypertrophy without exu-
date. Lungs, slight bronchitis and emphysema. Slight generalized enlargement
of lymph nodes. Blood pressure 125 systolic, 70 diastolic. Reflexes normal.
Pigmented scars on shins; sHght edema of ankles. Wassermann -j--|- in blood,
negative in spinal fluid. Physical examination otherwise negative.

Treatment. ^-On admission there was a rnoderate sugar and slight ferric chloride
reaction, and a heavy trace of albuminuria with large mmibers of hyaline and
finely granular casts. On Apr. 24, the first full day in hospital, the diet was 84
gm. protein, 3 gm. carbohydrate, and 2375 calories. Glycosuria entirely cleared
up during the day, and the ferric chloride reaction was also negative. Fasting
was begun, nevertheless, as the quickest means of undernutrition, and was con-
tinued for 8 days. The temperature and cough cleared up during this time, also
the albuminuria gradually diminished to a trace. The patient was fully com-
fortable, and on 450 cc. soup daily had no special complaint of himger. Green
vegetables were the first food given, in the form of a tolerance test. The gly-
cosuria with 20 gm. carbohydrate on May 4 was an accidental trace, not repre-
senting the true limit, which was reached with 100 gm. carbohydrate on May
8 and 9. This glycosuria ceased on cutting down the carbohydrate to 21 gm.
on May 10. Beginning May 11, two eggs and 50 gm. bacon were given as the
first substantial food in the 18 days since admission. 10 to 20 gm. carbohydrate
were retained in the diet, which was gradually built up to 65 gm. protein and 1330
calories on May 16 and 17. That this diet was too high was indicated by the
sharp rise in ammonia, and the high blood sugar on the morning of May 18.
The fact that glycosuria was absent then, but traces were present on certain
subsequent days, is possibly a phenomenon of renal permeability. Albumin
and casts were absent from the urine after May 9, and renal function tests by
Dr. McLean showed no abnormality throughout. It became possible to increase

344 CHAPTER III

all three classes of food rather rapidly. There was more feelipg of hunger toward
the close of May than on the fasting and lower diets previously. On May 13,
0.2 gm. salvarsan, and 0.5 gm. doses on May 24, and June 7 and 21, were injected
intravenously. There were 30 mercury inunctions about this time. At dis-
charge on July 7 the prescribed diet was 100 gm. protein, 95 gm. carbohydrate
(including 20 gm. bread), and 2400 calories (approximately 1.4 gm. protein and
33 calories per kg., reduced one-seventh by the weekly fast-days). The re-
covery of subjective health was complete, in such manner that there was no
question of the patient's future fidelity.

Acidosis. Ferric Chloride Reaction. — First may be noted the fact that a
slight ferric chloride reaction was present along with glycosuria on the lax diet
at admission, and on the carbohydrate-poor diet of Apr. 24 this cleared up com-
pletely. It then reappeared on the second day of fasting and became heavy,
but this was no reason for discontinuing the fast. The reaction diminished to
traces on May 8 and 9, but the ingestion of 100 gm. carbohydrate without other
food was unable to abolish it completely on these days. With the diminished
carbohydrate intake and the gradual addition of fat on the succeeding days, it
again became heavy, but showed the usual tendency to fade out, irrespective of
diet, as the general condition improved. After becoming negative, it stiU showed
the same tendency to reappear with fasting, being present on June 21 after a fast-
day (but not on the fast-day itself), absent with the fast-day of June 27, and
present on the fast-day of July 4. The trace of glycosuria which appeared on
Jime 23 was supposedly the result of slight excitement, and, as frequently hap-
pens, a trace of ferric chloride reaction appeared with the sugar.

Blood Bicarbonate. — No CO2 estimations were made during the first few days.
The low level of 45 per cent on Apr. 30 was probably the result of fasting. No
alkali was given, and the curve tended to rise rather than fall. Particularly the
allowance of a little carbohydrate brought it well up to normal limits on May 6.
With undernutrition and predominantly fat diet on May 12, the CO2 was again
down to 46.4 per cent. On the morning of May 18, following the increased diets
of May 16 and 17, it was again within normal limits. It may be noted that this
rise was not prevented by the febrile attacks mentioned below. On May 24,
following the preceding fast-day, it was again barely above 45 per cent. With
the higher diets and higher carbohydrate ration prior to discharge, the CO2
capacity was at a high normal level.

Ammonia.— In conformity with the absence of other signs of acidosis, the
ammonia nitrogen on carbohydrate-poor diet on Apr. 24 was only 0.63 gm. It
steadily rose on fasting, showing the development of acidosis, and on Apr. 30 had
reached 2.27 gm. The 100 gm. carbohydrate on May 8 and 9 brought the ammonia
down to a low normal level. Thereupon, with little carbohydrate, and under-
nutrition with a predommance of fat, the ammonia rose slightly. On May 13,
0.2 gm. salvarsan in 150 cc. saline was injected intravenously. On May 14,
there was temperature of 100.8°F., with slight albuminuria and a few casts!

CASE RECORDS 345

Toward evening there was a chill with temperature of 104°, leucocyte count
14,000, polynuclear 75 per cent; no malaria parasites; blood culture sterile;
influenza bacillus and Pneumococcus IV in sputum. On the following days
there was pain and swelling of the left leg from knee to ankle. By May 18, the
temperature was down to 99.2°, and thereafter was normal. Aside from the
hyperglycemia shown, this infectious attack made itself felt strikingly in the
ammonia output. This climbed steeply to the astonishing figure of 5 gm. am-
monia nitrogen on May 17, then fell abruptly as the temperature fell. Rela-
tively low values were present with the undernutrition and fasting of May 19
and 20. In consequence of protein-fat feeding, the ammonia rose as feeding was
continued to nearly 3.36 gm. N on May 26 and 30. Thereafter, with increasing
carbohydrate intake and improved general condition, the ammonia proceeded to
fall to a permanently normal level.

Blood Sugar. — The hyperglycemia doubtless present at admission was re-
placed by the normal figure of 0.120 per cent as early as Apr. 27. The rise to
0.167 per cent on Apr. 30 is one of the curious fluctuations which occur some-
times in fasting. Hyperglycemia of 0.168 per cent was present with the febrile
attack on May 18. Subsequent determinations showed fully normal values
(mornings before breakfast).

Weight and Nutrition. — The patient was obviously overnourished, and treat-
ment consisted primarily in reducing weight and relieving the overburdened
metabolism. The sharp fall in the weight curve during the early undernutrition
is shown in the graphic chart. It was noted above that only benefit was felt
subjectively, and the existing grippe infection and albuminuria both cleared up
promptly. Even during the period of low diets the patient said he felt as if 10
years had been subtracted from his age. He lost 10.2 kg. in hospital, but the
weight of 72 kg. at discharge was abundant for his stature, and he stated that he
had never felt better in his life. It is obviously bad practice to allow a diabetic
patient to carry abnormal weight. The good prognosis of fat diabetes belongs
to the mildness of the diabetes and not to the obesity, and the prognosis is better
when the obesity is properly reduced.

Subsequent History. — ^The patient took long vacation trips to Michigan and
California, exercised heavily in walking, swimming, etc., and remained free from
glycosuria. On Oct. 8 the diet was increased by two eggs and 20 gm. bread. The
weight was 72.6 kg. On Jan. 1, 1916, it was the same. On Apr. 8, 1916, 25
gm. glucose were given at 11 a.m., and specimens of urine at 12, 1, 2, and 3 p. m.
were negative for sugar. Weight 80 kg. On Apr. 24, the patient came to the
hospital fasting for the purpose of a glucose test. 100 gm. Merck anhydrous
dextrose were ingested at 9:55 a.m. The record was as follows:

346

CHAPTER III

Hr.

Blood Sugar.

Plasma Sugar.

Urine Sugar.

fer cent

fer cent

9:50 a.m.

0.125

0.135

0

10:50 "

0.179

—

0

11:50 "

0.156

0.164

Faint.

12:50 p.m.

0.123

0.110

0

2:05 "

0.083

0.084

0

Up to this time the patient had received a total of 9 intravenous injections of
0.5 gm. salvarsan and 30 mercury inimctions. The Wassermann reaction re-
mained consistently + + + +. With the idea that the diabetes might have
been of luetic origin and might have been cured by the specific treatment, per-
mission was given on the basis of this glucose test for the patient to relax his
diet to the extent of ceasing to weigh food, and merely take the same general
type of diet as before so as to avoid much carbohydrate. Up to June 1, 1916,
three more doses of salvarsan had been given, also three mercurial injections
outside this Institute. He was seen at the Institute July 14, weighing 86.2 kg.;
i. e., a greater obesity than at the time of the first admission. He looked tired
and overstrained. Glycosuria was present. He had not been performing urine
tests, and showed blood sugar 0.270 per cent, plasma sugar 0.294 per cent, CO2
capacity of plasma 62 per cent. He was instructed to resume a weighed diet of
93 gm. protein, 75 gm. carbohdyrate, and 2300 calories, and to take measures to
reduce his excessive weight. With swimming and other heavy exercise he lost
2 kg. in the following week, and became free from glycosuria and ketomu^ia on
July 20. On Jidy 21 the sugar in whole blood was 0.182 per cent, in plasma
0.204 per cent, COz capacity 54.7 per cent. The urine has since remained nor-
mal and the patient has retained subjective health. The management of the
diet at home is probably not accurate, for with continuous exercise he has never
brought his weight below 80 kg. Vigorous treatment with salvarsan and mer-
cury has been continued under the care of a competent private practitioner, but
the Wassermann reaction is stiU -f- -f- -|- in the serum.

Remarks. — The case is of special interest in connection with the possible
luetic origin of the diabetes. There has been no tendency to progress down-
ward even though the Wassermann reaction remained strongly positive. The
state of health was transformed by diet alone, before any antisyphUitic treatment
was employed. If specific treatment checked the syphilitic damage, it did not
repair it. The combined treatment did not cure the diabetes, notwithstanding
the excellent result of the glucose test of Apr. 24. It could then have been no-
ticed that the patient at his elevated weight showed hyperglycemia even on
fasting, and the blood sugar curve following the dose of glucose was unduly
high. This warning was not heeded; and with further gain of weight, without
carbohydrate excess, the inevitable glycosuria returned in due season.

The case was a t3rpical example of so called "spontaneous downward progress"
when the treatment was wrong; but progress was upward when the treat-

CASE RECORDS 347

ment was right. The patient's treatment of himself at home is evidently not
sufficiently stringent. He keeps his weight too high, and although he is in
excellent subjective health and carries on his work without difficulty and the
urine remains normal, more rigid treatment is necessary or there may ultimately
be trouble.'

CASE NO. 42.

Female, age 11 yrs. American; schoolgirl. Admitted Apr. 30, 1915.

Family History. — Patient is the only child of apparently healthy parents, with
no heritable disease anywhere in family as far as known.

Past History. — Measles and whooping-cough in infancy. Scarlet fever at 7
and again at 9. No sequelae. Has been a strong, healthy, well grown child,
though living in tenement environment. She has attended school in the usual
grades. During the past 2 years she has been nervous, the mother stating that
"the higher she gets in school the more nervous she gets." About the average
indulgence in candy. A curious feature of diet is that she has never eaten vege-
tables, not even potatoes. The food has been mostly eggs, bread, and milk.
Appetite has been notably small and she has had to be coaxed to eat.

Present Illness. — 3 weeks before admission polyphagia, polydipsia, and poly-
uria began acutely. After 2 weeks she was taken to a physician who first pre-
scribed carbohydrate-free diet with addition of milk, then as glycosuria continued
he advised bringing her to this Institute.

Physical Examination. — ^A thoroughly well developed and nourished, normal
appearing girl. Tonsils protrude and show deep crypts, with pus on pressure.
Very few small lymph nodes palpable. Reflexes normal. General examination
fully normal. The child is a splendid physical specimen, brimming over with hfe
and spirits.

Treatment. — Patient was admitted at 11:45 a.m. Apr. 30, and received no
food on that day. Castor oil was given as a laxative. The blood sugar was
0.286 per cent at 3:30 p.m., but probably diminished rapidly, for the glycosuria
in the mixed urine up to the next morning was only 0.3 per cent. On May 1,
nothing was given but two eggs and 450 cc. clear soup. May 2 and 3 were fast-
days. The glycosuria was only slight on May 1, and immediatelly cleared up,
the whole picture being characteristic of an early, still mild stage in which glyco-
suria and hyperglycemia had been kept up essentially by carbohydrate. On the
other hand, the ferric chloride reaction was well marked at admission and became
heavy on fasting. The child also vomited on the ist fast-day and was weak on

' Continued specific treatment finally reduced the Wassermann reaction to ± . .
At the same time continuous glycosuria gradually developed, followed within a
few weeks (Feb., 1918) by a rather threatening infection of the right foot. This
cleared up promptly with fasting and rest, and a more rigid dietetic regime has
since been pursued.

348 CHAPTER III

the 2nd. On May 4, she received 16 gm. carbohydrate without glycosuria.
With 40 gm. carbohydrate on May 5 in the form of green vegetables and 150 gm.
strawberries, a trace of glycosuria appeared, increased with 60 gm. carbohydrate
on May 6, and disappeared with a reduction of carbohydrate to 12 gm. on May 7.
By this time the ferric chloride reaction was diminished, and a diet of eggs and
sugar-free milk (Whiting's) was begun, with S gm. carbohydrate in the form of
celery and asparagus. The caloric intake was below 650, and with this under-
nutrition the ferric chloride reaction and all other signs of acidosis were cleared
up by May 13. Traces of glycosuria were frequent, and accordingly, without
further trouble from acidosis, the diet from May 16 to 21 was kept so low as to
represent almost continuous fasting. Beginning May 22, the attempt was made
to feed approximately 1200 calories daily; but glycosuria promptly appeared, and
continued notwithstanding withdrawal of carbohydrate and a partial fast-day on
May 27 and a complete fast-day on May 30. This being an impossible state of
affairs, the child was brought to confess that the glycosuria was due to her stealing
small quantities of bread. Though always a rather unmanageable patient,
she was tractable after learning that glycosuria meant fasting, and soon became
contented imder hospital discipline.

On Jime 2 partial, and on June 3 complete fasting was given. Beginning
June 4, a carbohydrate tolerance test was continued until June 26. A deceptive
trace of glycosuria appeared with 180 gm. carbohydrate on June 17, but the
true tolerance proved to be 260 gm. carbohydrate on June 25 and 26, in contrast
to the 40 to 60 gm. carbohydrate which had caused glycosuria on May 5 and 6.
The benefits of the 2 months of imdernutrition and liberal carbohydrate supply
were now apparent in a greatly increased tolerance for mixed diets. This was
rapidly built up, with routine weekly fast-days, and glycosuria was absent until
the increase reached 84 gm. protein, 110 gm. carbohydrate, and 2250 calories on
July 21. The ration was immediately reduced to a lower figure than had been
tolerated before, nevertheless glycosuria continued for 3 days. The child was
now clinically and subjectively entirely well, and the urine remained normal ex-
cept for the traces of glycosuria on Aug. 19 and 20, due to stealing food. Oct. 11
to Nov. 3, another carbohydrate test showed a tolerance of 240 gm., as compared
with 260 gm. in June. In Nov. a diet of 75 gm. protein, 75 gm. carbohydrate,
and 1500 calories was assimilated without glycosuria. In Dec. the attempt to
replace part of the fat with carbohydrate, making the diet 75 gm. protein, 100
gm. carbohydrate, and 1500 calories, was endured for about 2 weeks, then caused
glycosuria on Dec. 15 and 16, so that the former diet with 75 gm. carbohydrate
was resumed. She was discharged on this, after having been 232 days in
hospital.

Acidosis. — This was an instance of the production of acidosis by fasting.
The tendency was already present, as shown by the ferric chloride reaction and
slightly subnormal blood alkalinity at admission; but the nausea and weakness
developing early in fasting were characteristic, and on the morning of May 4

CASE RECORDS

349

the CO2 capacity of the plasma was found to have fallen to the ominous level of
27 per cent. No alkali was given, but only the 16 gm. carbohydrate in green
vegetables as mentioned. With small carbohydrate intake the CO2 capacity
rose quickly to 44 per cent on May 6; then on a protein-fat diet of 600 calories
with only 5 gm. carbohydrate it rose still further. On May 18, which was a
green day with 20 gm. carbohydrate in the form of celery, asparagus, tomato,
and cucumber, the CO2 was as high as at admission. With the carbohydrate
tolerance test in June it reached a high normal level. It tended to fall below
normal on the ensuing mixed diet. The tendency toward acidosis on fasting was
displayed in the tests made on the morning of the fast-day of Sept. 12 and the fol-
lowing morning, but the steep drop in plasma bicarbonate as a result of this
fast was partly explainable by the lively exercise which the patient was now
taking. The later values, with the exception of the low figure of 48.8 per cent
on Nov. 17, were normal for a child.

Blood Sugar. — The quick fall to normal is characteristic of an early case.
Normal values were still present on Sept. 12 and 13, after a long period of ade-
quate nutrition; but increase of the carbohydrate allowance from 82 to 100 gm.
on Sept. 23 without change in the total calories resulted in a rise of blood sugar
to 0.26 per cent on Oct. 7. There was hyperglycemia of 0.25 per cent on Oct.
22 during the carbohydrate test. Thereafter the general tendency of the curve
was downward. Notwithstanding the increase of carbohydrate on Nov. 30,
which subsequently resulted in glycosuria, the analysis before breakfast on Dec.
4 showed normal sugar in the whole blood and only slight elevation in the plasma.
At the close of the following week, on Dec. 11, there was definite hyperglycemia,
giving advance warning of the glycosuria which appeared on Dec. IS.

Weight and Nutrition. — Though the patient was a growing child, undernu-
trition was employed to obtain control of the threatening condition present when
admitted. The degree of undernutrition thus enforced for 2 months can be
shown as follows. The quantity of bread obtained surreptitiously was so small
as to be negligible in this calculation.

58 days.

Total calories in diet 37,132 0

" protein" " 1,769. 9gni.

Animal " " " 850.3 "

Vegetable" " " 919.6 "

Carbohydrate" " 3,190.0 "

Per day

(average)

Per day

per kg.

640.0

24.0

30 . 5 gm.

1.13 gm

14.6 "

0.54 "

15.8 "

0.58 "

55.0 "

2.03 "

The child was cross and rebellious at first because of having been spoiled at
home, so that trouble resulted not merely from hunger but from any matters in
which her will was thwarted. The greatest loss of weight was 3 kg. The in-
crease of weight during the carbohydrate test in June represented the usual
slight edema. By reason of the subsequent diets, the weight at dismissal was the
same as at entrance. It was not learned whether any growth in stature occurred

350 CHAPTER III

in hospital. At discharge, with weight of 27 kg. and height of 129.8 cm., the child
appeared splendidly developed and nourished and her strength and spirits were
of the highest.

The diet at discharge represented approximately 2.8 gm. protein and 56 cal-
ories per kg., reduced by the weekly fast-days to 2.4 gm. protein and 48 calories
average per kg. Along with this, heavy exercise had been employed and was
evidently one reason for the failure to gain weight. The child had certainly
gained in muscle, for her muscles were large and hard at discharge, and presum-
ably she had lost some fat. Exercise was in the form of strenuous sports, and
because of her strength and boisterous disposition she enjoyed these thoroughly.

Subsequent History. — This was an instance in which more reliance had to be
placed on the child than on the parents, for they would not control her effectively.
Though spoiled and rebellious at first, she had become obedient and convinced of
the necessity of remaining free from glycosuria. Though in tenement environ-
ment, she was able to obtain the required food, and remained free from glycosuria,
except for 1 day in Jan. with a bad cold. She continued exercise and also at-
tended school, leading a thoroughly normal child's life except for diet. On
Mar. 2, 1916, the height was 130.6 cm. On Apr. 18, the blood sugar was 0.156
per cent, plasma sugar 0.164 per cent, CO2 capacity 52.6 per cent. As the urine
was consistently normal, 150 cc. milk were added to the diet. On June 13, the
blood sugar was 0.123 per cent, plasma sugar 0.130 per cent, CO2 capacity 52.1
per cent. On July 17, the health and urine remained as before. The blood sugar
was 0.192 per cent, plasma sugar 0.227 per cent, CO2 capacity 50.5 per cent.
Weight 26.8 kg. Height 131 cm. The diet was diminished to 1400 calories
with only 50 gm. carbohydrate, and the patient was allowed to go to the country
until fall. In Nov. traces of glycosuria began to appear frequently, the urine and
subjective condition having been normal up to this time. The patient was there-
fore readmitted Nov. 17, 1916.

Second Admission. — The weight was 27.8 kg. There was slight edema of feet,
but the apparent physical condition was still very good, though the child was
obviously not so strong as before. Only a trace of glycosuria was present, but
this persisted on a diet of 60 gm. protein, 15 gm. carbohydrate, and 800 calories.
It cleared up with 1 fast-day. A carbohydrate tolerance test was then insti-
tuted in the usual manner, and the tolerance was found to be only 90 gm. There-
after a diet was given consisting of '40 gm. protein, 10 gm. carbohydrate, and
800 calories. Any attempt at an increase above this diet caused glycosuria.
She was discharged on this diet Dec. 18, 1916, weighing 25.5 kg. On the basis of
this weight, with allowance for the weekly fast-days, the prescribed diet repre-
sented 1.3 gm. protein and 27 calories per kg.

Subsequent History. — Traces of glycosuria still recurred, and on this account
the patient was out of the hospital only a little over 2 weeks.

Third Admission. — Jan. 4, 1917. Weight 27.5 kg., evidently explainable by
edema, as the diet had not been high enough for gain in weight. Only a trace

CASE RECORDS 351

of glycosuria was present, and the prescribed diet was continued for 3 days in hos-
pital to determine whether it resulted from violation of diet at home. The
sugar, however, slightly increased instead of decreasing, and 2 fast-days were then
necessary to stop it. The trace of ferric chloride reaction present at admission
persisted on fasting, but the ammonia nitrogen, which had been 1 gm., fellto
0.36 gm. A carbohydrate test was then given in the usual manner, and the toler-
ance was found to be only SO gm., indicating steady downward progress. The
blood sugar on admission was 0.332 per cent, and at the end of a fast-day following
the carbohydrate test it was 0.176 per cent. Frequent traces of glycosuria and
acidosis persisted on a diet of 36gm. protein, 10 gm. carbohydrate, and 750 calories.
In Feb. the condition changed for the worse. There were gastric upsets, edema
of face and legs', mental depression, and loss of weight and strength. The diet
was gradually diminished to 25 gm. protein and 350 calories without carbohy-
drate, but traces of glycosuria continued, while acidosis was absent or slight by all
tests. There was no cough, but pain particularly with breathing appeared over
the precordia. The temperature did not go above 98.9° F. Physical and x-ray
examinations gave only suspicious and not positive signs in lungs. The continu-
ance of pain made tuberculous pleurisy probable. On Feb. 27, the CO2 capacity
of the plasma was down to 44 per cent. A trace of ferric chloride reaction re-
turned on Mar. 5. At the beginning of Mar. the attempt to maintain sugar-
freedom was abandoned, and heavy glycosuria was thenceforth present on a
carbohydrate-free diet of 30 gm. protein and 450 calories. By Mar. 8, the am-
monia nitrogen was up to 1.1 gm. The ferric chloride reaction gradually became
heavy. By Mar. 14 the ammonia nitrogen was 1.5 gm. The CO2 capacity of
the plasma was 18.9 per cent on that day. IS gm. sodium bicarbonate were
given, and the CO2 capacity fell to 16.9 per cent. The patient died in diabetic
coma on Mar. 15, 1917.

Remarks. — The patient was received with diabetes acute and severe in type,
but yet early and mild in degree. She was treated for 2 months with rigorous
undernutrition, and all threatening symptoms cleared up and a high carbohydrate
tolerance was developed. Undernutrition was then abandoned and the attempt
was made to feed a high calory diet suitable for a normal child, while at the same
time gain in weight was prevented by means of heavy exercise. A splendid physi-
cal condition was attained.

The child was kept alive for 2 years, during the greater part of which she
enjoyed a high degree of health and led an approximately normal existence. The
outcome shows that exercise cannot wholly replace restriction of total calories.
While downward progress may be unavoidable with severe diabetes under the
metabolic strain of youth and growth in children, a longer and better course in
other children more rigidly treated is an indication that at least part of the down-
ward progress in this case was attributable to the unduly high diet. It is better
to make a less severe reduction in the earliest stage when so much greater benefit
is attainable, than a more extreme reduction after downward progress has

352 CHAPTER in

resulted. As usual, the attempt to maintain the highest possiblelevel of vigor
did not prevent and probably predisposed to infection. With the onset of
tuberculosis, a quickly fatal termination in such a case was assured.

CASE NO. 43.

Female, xmmarried, age 27 yrs. American; nurse. Admitted May 31, 1915.

Family History.— Fa.theT died at 70 of Bright's disease. Mother died of un-
known cause during menopause at 45. Possible diabetes in a maternal aunt.
Maternal grandmother died of tuberculosis. No other heritable disease known.

Past History. — Patient has spent her life under favorable conditions in two
southern states. In childhood, measles, mumps, whooping-cough, chicken-pox,
diphtheria. Pneumonia at 7 and again at 17; both light. In the spring of each
year she has had so called malarial attacks with slight fever and malaise, but
without chills. Menstruation has been irregular. General health good. Habits
and diet normal. 3 years ago she accidentally plunged a hj^odermic needle
into her hand and broke off the point, which was not extracted for 24 hours.
Severe sepsis resulted. The whole arm was swollen and blackened, and three
incisions were made for drainage. There was delirium, and at one time her
recovery was not expected. The hand has only partially recovered function.
There was also albuminuria durilig the attack, and treatment with diet and
other measures for nephritis was followed for many months. Albuminuria finally
cleared up.

Present Illness. — In Jan., 1915, marked polyphagia, polydipsia, and polyuria
were noticed, and the weight fell from the usual 118 to 97 pounds. About the
first of Mar. she concluded she had diabetes, and this was confirmed by a medical
examination. Beginning late in Mar. she was imder treatment in hospital for
several weeks on the von Noorden plan with green days, oatmeal days, and
occasional fast-days. She was sugar-free during the last week, but relapsed on
leaving hospital. Since the middle of Apr. she has been on protein-fat diet with
addition of green vegetables, a little potato, and two slices of bread at each meal.
Pruritus vulvae troublesome.

Physical Examination. — ^Poorly developed, thin young woman. Pale com-
plexion. Skin dry. Considerable loss of hair. Mouth and throat normal. A
few barely palpable lymph nodes. Reflexes normal. Trace albuminuria. Ex-
amination otherwise negative.

Treatment. — On June 1, the first day in hospital, the diet was 83 gm. protein,
5 gm. carbohydrate, and 2530 calories. The sugar excretion was 14.88 gm. On
the next day 2071 calories were taken. June 3 and 4 were fast-days with no food
of any kind. On June 5 and 6, 300 cc. clear soup, 150 cc. coffee, and 3550 cc.
whisky were permitted. Glycosuria cleared up, but signs of acidosis became
marked. On June 7, green vegetables containing 10 gm. carbohydrate produced
prompt glycosuria. This carbohydrate was continued, and eggs, butter, and

CASE RECORDS 353

bacon were added to build up a diet approximating 1600 calories. Glycosuria
diminished when the carbohydrate was halved, but did not cease until the fast-
day of June 13. Thereafter a similar diet was tolerated up to June 21. Begin-
ning June 22, a carbohydrate tolerance test was instituted, and ignoring insignifi-
cant traces of glycosuria on July 5 and 8, the tolerance was reached with 230 gm.
carbohydrate on July 17 and 18. Thereafter a mixed diet of 80 to 100 gm. pro-
tein, 100 gm. carbohydrate, and 2200 to 2500 calories was taken, with only occa-
sional traces of glycosuria. The weight having risen to equal that at entrance,
another carbohydrate test was begun on Oct. 11, and the limit of tolerance was
reached with 170 to 190 gm. carbohydrate. Mixed diet was then resumed, and
though 2500 calories were tolerated, the permanent level, beginning Nov. 5,
was fixed at 2000 calories. Green days with 25 gm. carbohydrate were substi-
tuted for the previous weekly fast-days. Though glycosuria was absent, the
carbohydrate allowance beginning Nov. 26 was diminished to 25 gm. Never-
theless, a decided glycosuria appeared in the middle of Dec. It was then learned
that this, and also the preceding appearances of glycosuria (Nov. 6 to 24) had been
due to the patient's buying and eating 10 cents worth of cheese when on walks
away from the hospital. After reduced diet and fasting (Dec. 17 to 20) the gly-
cosuria was cleared up, and the former diet resumed on Dec. 21 without glycosuria.
The patient was dismissed on a diet of 80 gm. protein, 25 gm. carbohydrate,
and 1800 calories (1.92 gm. protein and 43 calories per kg., reduced by weekly
fast-days to an average of 1.65 gm. protein and 37 calories per kg.). She felt
well at discharge, except on fast-days, which always left her temporarily weak
and depressed. She proposed to imdertake diabetic nursing, and was instructed
also to continue regular exercise.

Acidosis. — ^At admission there were no acidosis symptoms, the ferric chloride
reaction was slight, the ammonia output was low, and the first carbon dioxide
determinations only slightly subnormal. Acidosis was produced by fasting. The
ferric chloride reaction promptly became heavy. Before breakfast on the morning
of June 7 the CO2 capacity of the plasma was down to 35 per cent, and the am-
monia nitrogen by that day had risen to 2.35 gm. Alcohol up to 350 calories had
not prevented this acidosis. On June 8, 20 gm. sodium bicarbonate were given,
with the low calory diet and 10 gm. carbohydrate above mentioned. The result
was a prompt rise in CO2 and fall in ammonia. But with simple increase of pro-
tein-fat diet without any more alkali, the CO2 capacity rose still more sharply
to a fuUy normal level, and the ammonia output correspondingly fell. The
acidosis was also manifested by the usual clinical symptoms of nausea, vomiting,
and malaise; these also cleared up promptly on feeding. The CO2 capacity was
unaccountably low on July 8, probably in consequence of undernutrition and
exertion, while on the next day the usual high normal value was found present.
On mixed diet the curve had descended by Sept. 12 to the lower normal limit.
The tendency toward acidosis on fast-days persisted. Sept. 12 was a fast-day,
and the CO2 capacity that morning was 54.8 per cent, whereas the next morning,

354 CHAPTER III

after 24 hours with only 300 cc. soup and 300 cc. coffee, it was down to 46.6 per
cent; while after 3 days of feeding it was 57 per cent on the morning of Sept. 16.
It was also within normal Hmits on Oct. 29, at the close of a carbohydrate test;
but on the morning of Nov. 1, after the previous fast-day, it was down to 47.4 per
cent. On the other hand, on Dec. 19 the high normal value found after fasting
is perhaps one indication of the improved condition, notwithstanding the exist-
ence of a positive ferric chloride reaction in the urine at that time. It is also
worth noting that the ferric chloride reaction became negative on June 28 with
nothing in the diet but vegetables representing 70 gm. carbohydrate. But after
the carbohydrate test it reappeared on mixed diet in July and Aug., notwith-
standing 100 gm. carbohydrate in the diet. Thereafter it tended to reappear,
particularly with glycosuria. It seemingly was governed not so much by the
carbohydrate intake as by the fat in the diet and the specific diabetic condition.

Blood Sugar. — The hjrperglycemia found on the morning of Sept. 12 was
promptly reduced to normal by the single fast-day. It was again unduly high
with feeding, but showed a downward tendency. The excessive figure of 0.4
per cent in whole blood and 0.44S per cent in plasma at the close of the carbo-
hydrate test on Oct. 29, .with only slight glycosuria, probably indicates renal im-
permeability, perhaps associated with the old nephritis. At the same time it
must be borne in mind that the urine reactions are shown for the 24 hours, whereas
the blood sugar was for the hyperglycemia during carbohydrate digestion. On the
morning of Nov. 1, it was found that a single fast-day had again brought the
blood sugar fully to normal. On Nov. 13, it was 0.125 per cent in whole blood and
plasma, and was barely below 0.15 per cent on Dec. 19 in consequence of the
recent violation of diet.

Exercise. — ^As soon as adequate mixed diet was begun in Aug., vigorous exercise
was inaugurated, including daily walks of 8 mUes. The strength and general
appearance thereby improved. Glycosuria was present on Sept. 11, just before
the routine fast-day. Exercise was then omitted, and it appeared earlier in the
following week; namely, on Sept. 14 and IS. Without change in diet, an increase
of exercise was ordered, and glycosuria immediately ceased and remained entirely
absent in the subsequent weeks up to Oct. 9. Other observations concerning
exercise, particularly the blood sugar, are given elsewhere (Chapter V).

Emotion. — The glycosuria of Aug. 10 and 11 was apparently associated with
crying spells.

Weight and Nutrition. — The weight at admission was 44 kg. Some of the fluc-
tuations in the curve, notably the rise during the carbohydrate test in July, were
due to edema. It is noteworthy that the toleratice in Oct., after recovery of the
original weight, was far different than at admission, but yet was lower than in
July. It seems clear that the high diets from July to Oct. had been injurious,
notwithstanding the use of exercise. At discharge the weight was 41.6 kg.;
i.e., a loss of 2.4 kg. This was 12 kg. below her normal weight, and she had
always been rather shght in figure. The above mentioned diet, prescribed at

356 CHAPTER in

patient never was guilty of any large violation of diet, but indulged herself in
little things beyond permission. Glycosuria occasionally returned, and finally
became continuous. When she began to feel rapidly worse, she returned for
readmission on Dec. 2, 1916.

Third Admission.— Tht weight was 39 kg., partly edema. No acute symp-
toms were present, but there had been a perceptible loss in strength. With 3
days of fasting, sugar and ferric chloride reactions became negative. The diet
was then built up in the usual maimer, and the tolerance was found very low.
The limit was approximately 1000 to 1100 calories with 50 gm. protem and no
carbohydrate, and with the usual weekly fast-days. A considerable part of
this long period in hospital was occupied with tests with fat feeding, some of
which are described elsewhere (Chapter VI). On the very low diet the weight
has fallen to about 33 kg. The strength also is diminished, so that the patient
is now a confirmed invahd, able to be up and about, but not fit for work or for an
independent existence. She has remained in the hospital iip to the present.

Remarks. — The record of this patient during and following the first hospital
period confirms the fact that exercise cannot atone for an unduly high diet
The essential reasons for her downward progress have been the almost per-
petual, slight overstepping of diet, and the frequent colds and grippe. She has
reached the point where nothing but a hard struggle for the bare maintenance of
Ufe is possible. With continuous hyperglycemia not tending to diminish, a slight
continuous overstrain of the pancreatic function may be assumed, and down-
ward progress may be expected imder such conditions even in the absence of in-
discretions or compHcations. The only hope Hes in treatment radical enough
to relieve the overstrain if possible. The later results wUl show whether down-
ward progress can thus be checked at such an extreme stage.

CASE NO. 44.

Male, married, age 33 yrs. American; electrician. Admitted July 3, 1915.

Family History. — Parents hved to old age. Wife and three children of patient
are well. One aunt died of cancer of the nose. History otherwise negative.

Past ffwtory.— Diphtheria at 4. Frequent colds m head but no cough or sore
throat. Gonorrhea 11 years ago. Syphihs denied. Has worked in electrical
power house for past 15 years, for past 3 years as switchboard attendant. Mod-
erately nervous and excitable. No alcohol except occasional glass of beer.
Smokes considerably. Four or five cups of tea or coffee daily. Not a heavy
eater in general, but a lover of sweets. Highest weight 170 pounds, average 165
pounds clothed.

Present Illness. — ^Headaches and lassitude began about a year ago. 5 months
ago pleurisy with chills, cough, and bloody expectoration confined him to bed
for 10 days. Weight has been steadily lost, and there have been night sweats for
week preceding admission. Polydipsia and polyuria began shortly after the

CASE RECORDS 357

pleurisy. A physician then diagnosed diabetes. In addition to medicines, he was
given a diet restricted to protein-fat foods with gluten bread and such vege-
tables as grow above the ground. He continued to lose steadily; impaired hear-
ing, numbness of hands and feet, cramps in legs at night, nervousness, and
irritability have been present.

Physical Examination— Height 175 cm. A fairly developed, moderately
emaciated man without acute symptoms. Slight pyorrhea. Many teeth miss-
ing. Tonsils not enlarged. Slight lymph node enlargements. Reflexes normal.
Blood pressure 90 systolic, 62 diastolic. Wassermann negative. Examination
otherwise negative.

Treatment.— Jinmig the first few days in hospital, glycosuria and ketonuria
were heavy on a diet of 2100 to 2400 calories with S gm. carbohydrate. The in-
crease of carbohydrate to 40 gm. on July 7 made little difference. On July 8,
only breakfast was given, and glycosuria cleared up during the day. 3 fast-days
were then imposed nevertheless, followed by a carbohydrate period. An intake
of 340 gm. carbohydrate in the form of green vegetables was reached without
glycosuria. The ferric chloride reaction meanwhile became negative. After a
fast-day on Aug. 1, the diet for 3 days was limited to potato, and 200 gm. carbo-
hydrate were taken in this form without glycosuria. A mixed diet was then
given, consisting of 100 gm. protein, 100 gm. carbohydrate, and 2600 calories.
Ferric chloride reactions promptly appeared, and persisted notwithstanding in-
crease of catbohydrate to 285 gm. on Aug. 21. The diet on this day also con-
tained 130 gm. protein and 3100 calories. Of this carbohydrate, 40 gm. were in
the form of bread and 100 gm. in the form of potatoes. The patient was dis-
charged on Aug. 23, weighing 58.6 kg., on a prescribed diet of 115 gm. protein,
160 gm. carbohydrate, and 2700 calories (almost 2 gm. protein and 50 calories
per kg., reduced one-seventh by weekly fast-days).

Acidosis. — The CO2 capacity of the plasma was sUghtly below normal, and rose
steadUy under treatment without the aid of alkali. The most interesting feature
from the standpoint of acidosis pertained to the ferric chloride reaction, for al-
though this became negative on a solely vegetable diet, it reappeared on a liberal
mixed diet, notwithstanding an ingestion of carbohydrate theoretically abundant
to prevent all acidosis.

Subsequent History. — The patient resimied his regular work, and maintained
health and normal urine. On Oct. 5, both sugar and ferric chloride reactions
were absent from the urine, and the sugar in whole blood was 0.102 per cent, in
plasma 0.110 per cent, weight 61 kg. In addition to his regular work of 8 hoiurs
a day he was making extra money and at the same time obtaining exercise by
canvassing several hours daily. On Dec. 27, the patient reported at the Insti-
tute with temperature of 99.2° F., after having had grippe and precordial pain for
10 days. Acidosis remained absent and he had continued his regular work. The
excessive diet was reduced to 97 gm. protein and 2170 calories. The grippe
cleared up promptly, and later examinations showed lungs and urine normal.

358 CHAPTER m

Secoftd Admission.— On Apr. 26, 1917, the patient was readmitted on account
of lobar pneumonia (Pneumococcus Type IV). Physical signs and radiograms
indicated consoUdation of right middle lobe. The temperature on adm'ssion
was 101°F., rose the next day to 104°, on Apr. 28 reached the maximum of 105.6°,
was still as high as 105.2° on Apr. 29, and fell by crisis to normal the next day.
Liquid diet was given, largely milk, containing as high as 40 gm. carbohydrate. ^

The course of the pneumonia was uneventful, and neither glycosuria nor acidosis
appeared. The patient was transferred from the pneiunonia to the diabetic serv-
ice on May 5. He convalesced uneventfully, and was discharged May 28 on a
diet of 100 gm. protein, 80 gm. carbohydrate, and 2250 calories. Weight 59.2 kg.

Subsequent History.— On June 19, the patient caught cold and also lost his
temper in a dispute. Rather heavy glycosuria appeared promptly, but disap-
peared on omitting four meals. On resinning full diet glycosxu-ia returned, and
ceased with another fast-day. The patient then reduced h s diet and reported
on July 2, having been sugar-free s'nce the attack. The diet was ordered di-
minished to 80 gm. protein, 60 gm. carbohydrate, and 2000 calories. On this he
has since remained shghtly himgry but free from symptoms and feeling strong
and well. In July, 1917, the weight was 61.9 kg., the blood sugar during digestion
0.112 per cent, CO2 capacity 60.2 per cent.

Remarks. — ^The diabetes was essentially mild, and it is hoped that it may be
kept so. The most noteworthy feature is the wholly uneventful manner in which
the patient passed through an attack of pneumonia of moderate severity. The
absence of diabetic symptoms during this time may be attributed chiefly to the
very low diet given during the period of active infection. Permanent injury
of the tolerance was thus apparently prevented. Notwithstanding the excellent
condition and the normal blood sugar, the outbreak in June shows that the latent
diabetes must stiU be guarded against, doubtless throughout the patient's life,
though improvement may perhaps continue with advancing years. On the
other hand, the age is such as to threaten serious consequences if the condition is
not held in check. The patient is now on a well balanced diet, which may be ex-
pected at least to delay any downward progress if it does not prevent it altogether.

CASE NO. 45.

Male, age 6 yrs. American Jew. Admitted Sept. 1, 1915.

Family History.— Pa.Tents and two brothers of patient (aged 9 and 11) are en-
tirely well and free from glycosuria, though shghtly obese. No diabetes in
mother's family, but her mother died of cancer at 53. The father's family his-
tory is negative on his mother's side, but diabetic on his father's side; i.e., a
great grandmother died at 76 of diabetes, and the father and an uncle of the
present patient's father are living and have diabetes. No tuberculosis, syphilis,
Bright's disease, goiter, etc., known.

CASE RECORDS 359

Past History. — Normal delivery. No childhood diseases; never sick a day.
Always big and plump, but not obese. Never nervous. Has never gone to
school but received a little instruction from a governess. He has been bright
and quick to learn, and has spent nearly all his time playing, automobUing, or in
other active recreations. Appetite always large, and he has eaten much cake,
candy, ice cream, and other sweets.

Present Illness. — ^About Nov. 20, 1914, polyuria and loss of weight were no-
ticed. A physician prescribed medicine without examining the urine. Another
physician a few days later discovered glycosuria, and two eminent consultants
were called. A repetition of oatmeal and green days was employed according
to the von Noorden plan, and the patient with difficulty was made free from
glycosuria, but acetonuria persisted. Last Mar. there was an attack of grippe,
with otitis media requiring paracentesis, which was performed without anesthesia.
The patient is said to have become completely comatose; he was treated with
fasting and rectal drip, recovered from this attack, and became sugar-free on a
diet of Whiting's milk and thrice cooked vegetables. A little carbohydrate was
later added, but traces of acetone continued. During the past summer, at the
parents' summer home, the control was too lax to prevent violations of diet, with
the result that on July 10 the patient suddenly fell out of his chair at table. He
was then brought to New York and placed imder the care of one of the advocates
of treatment with lactic acid bacilli. A fuU caloric diet was given with restricted
carbohydrate during this treatment, and also sodium bicarbonate, from one to
six heaping teaspoonfuls daily. There was steady loss of weight and strength.
For 7 weeks past the patient has been confined to bed or chair, unable to stand
because of weakness; for past several days he has been too weak to sit up. Dur-
ing this time apathy and stupor have been increasing, but he is not quite in
coma. Greater edema than that now present is said to have occurred from bi-
carbonate in the past. The weight before onset of diabetes was 47 pounds; be-
fore the present bicarbonate edema, it was 36 pounds. Meantime a long series of
urinalysis reports from a commercial laboratory, exhibited by the father, showed
steady improvement under the lactic acid treatment, the glycosuria being dimin-
ished from heavy to slight and the acidosis having disappeared. The practi-
tioner in charge blamed the laboratory for the mistake, but had been administer-
ing sodium bicarbonate in maximum doses rectaUy as well as orally. An incon-
sistency on the part of the laboratory was that their reports showed acid reac-
tions of the urine with alleged negative ferric chloride reactions imder this
treatment.

Physical Examination. — Patient stiU shows signs of having been a splendidly
developed, handsome child. He is now stuporous, and questions must be re-
peated several times before a response is obtained. Complexion pasty. High
degree of general anasarca; deep pitting of extremities on pressure, and fingers or
bed clothing leave marks all over the body. EyeUds are swelled nearly shut.
Intraocular pressure very low. Mucous membranes very red; tongue coated;

360 CHAPTER in

gums swollen and spongy and bleed easily. Throat not examined because of
mental condition and edema. No gland enlargements made out. Left chest
hjrperresonant. Right side shows everywhere flatness and other signs of a
large pleural effusion. Systolic blood pressure approximately 62. Marked
tympanites in abdomen, and movable dulness in flanks. Both testicles in
scrotum, partly obscured by fluid which swells scrotum to about the size of a
large apple. Knee and Achilles jerks not obtainable. Over the sacrum an area
of dusky redness, as large as a man's hand, seems almost ready to slough. Tem-
perature 97.4; pulse 66; respiration 16, without dyspnea.

Treatment. — (No graphic chart.) The patient was too weak to move himself
in bed, and the nurses were instructed to turn him at intervals with a view to
avoiding pressure sores and h)rpostatic pneumonia. Fasting was begun with
very small doses of whisky. Notwithstanding the huge bicarbonate edema, the
previous reports of acid urine were confirmed, and in the presence of incipient
coma, fear was entertained of stopping bicarbonate suddenly, or using any strong
diuretic which might alter the water balance in imknown manner. Accord-
ingly, on the 1st day 10 gm. sodium bicarbonate, 16 gm. calcium carbonate, and
4 gm. magnesium oxide were given, and on the next day 20 gm. each of sodium
bicarbonate and calcium carbonate, also 1 cc. aromatic cascara. Satisfactory
laxative action was obtained, and there was neither nausea nor diarrhea. The
tympanites was reheved. The attempt was made to force fluids, and 3850 cc.
water were given on Sept. 2, but the total urinary output was only 1425 cc. It
was evident that the child was unable to dispose of his fluid, and this fact was
further evidenced by the gain of 2.6 kg. weight, with evident increase of edema.
Strength did not improve, as it frequently does on fasting. On the contrary,
there was a perceptible increase of weakness, though the mental condition decid-
edly improved. Both glycosuria and ketonuria were rapidly diminishing. Be-
ginning Sept. 3, no alkali was used, and water was suppUed only for thirst. By
Sept. 5 glycosuria was absent, and on the next day the ferric chloride reaction
was entirely negative. The child was mentally bright, and seemed in no imme-
diate danger in regard to strength. Green vegetables representing 3.3 gm. car-
bohydrate were eaten with reUsh, and it was planned to begin protein feeding the
following day, with encouraging prospects. Edema was beginnmg to subside, as
shown by the falling weight; but albuminuria, which had been absent on admis-
sion, seemed to develop as the urine turned alkaline; casts were not foxmd. Dur-
ing the night of Sept. 6-7, the strength suddenly collapsed altogether. The resi-
dent physician, immediately called, gave a saline hypodermoclysis, which was
absorbed but had no perceptible effect. When seen at 4:30 a.m., the child was
cold in spite of being surrounded with hot water bottles; temperature down to
95.8°; pulse 60, barely perceptible; respiration 16 to 20; completely unconscious,
without eye reflex; rectal sphincter completely relaxed. 10 gm. levulose m 100 cc.
water were immediately given by stomach tube, and another 10 gm. in 100 cc.
saline subcutaneously. The condition seemed to improve sHghtly, but con-

CASE RECORDS 361

sciousness did not return. At 6:50 a.m. another hypodermoclysis was given of
250 cc. saline containing 20 gm. levulose. Half an hour after this, when asked if
he was hungry, the child answered yes. He swallowed 50 cc. bouillon containing
2 gm. ereptone. During the day six eggs, SO gm. butter, and 700 cc. soup were
taken with relish, also 20 cc. whisky. A similar diet was given on Sept. 8.
The child seemed to be rapidly gaining strength; but diarrhea was present, sup-
posedly due to the levulose and ereptone, and bismuth was given for this. By
Sept. 9, the stools had become frequent, badly digested, and very putrid in odor.
Tympanites had returned. In place of the former subnormal temperature there
was now fever of 101.8°. The blood pressure could now be definitely determined
at 85 systolic and 68 diastolic. The patient now moved his arms and legs volun-
tarily, but had not become able to turn his body. On account of the apparent
putrefactive intestinal condition, and the impossibility of employing fasting in
view of the former collapse, it was decided to try oatmeal. Therefore, the former
egg diet was stopped after breakfast. A dose of 10 cc. castor oil was given; 16
cc. whisky, 60 gm. oatmeal, and 200 cc. clear soup constituted the diet for this
day. The tympanites and diarrhea were not relieved; stools became frothy as
well as foul smelling. Heavy glycosuria appeared immediately, as shown in Table
XII, and with it a moderate ferric chloride reaction. Stupor and Kussmaul
dyspnea came on rapidly. As the oatmeal had failed so completely, it was or-
dered stopped at evening, and 10 cc. more castor oU were given. Between 9
and 10 p.m., a 250 cc. cylinder containing 25 cc. 3 per cent sodium citrate solu-
tion was filled with blood from the patient's father. A vein was exposed in the
patient's arm, the operation eliciting no sign of consciousness, and the blood was
■allowed to flow in. It was hoped by means of the transfusion to contribute a little
strength to tide over the fasting necessary as the only hope for clearing up the
coma. No inmiediate change was perceptible except a slight improvement in
pulse. On Sept. 10, the temperature had become normal and the patient could
be roused. Toward evening he wakened spontaneously and began to cry for
food. 75 cc. clear soup were given. Edema of both face and feet became more
marked. On Sept. 11, the child became unconscious in a different manner,
with weak pulse and feeble Cheyne-Stokes breathing. Another transfusion of
150 cc. citrated blood from the father was given; a hypodermoclysis of 200 cc.
saline containing 10 gm. levulose; and by stomach tube 6 cc. whisky, 10 gm.
levulose, and 140 cc. Whiting's milk, from which the cream had been removed
by centrifugation. The temperature was normal, and the picture was one of
intoxication, different from the previous hunger collapse or diabetic coma. Eggs
and whisky were given by stomach tube during the day, making a total diet of
40 gm. protein and 500 calories. The putrid smelling diarrhea returned, and
death occurred with weakness, imconsciousness, and Cheyne-Stokes breathing at
5:30 p.m.

Acidosis. — ^The excessive use of bicarbonate, guided only by the urinary reac-
tions, had produced not only extreme anasarca but a decided alkalosis. Prob-

362 CHAPTER in

ably this and the renal impermeability formed a vicious circle, each making the
other worse. The lack of paralleUsm between urine and blood is illustrated by
the acid urine of Sept. 9, with the highest plasma alkalinity of the series. The
value of the direct determination of the plasma bicarbonate is thus illustrated.
The only other indication that no more alkali was needed was given by the low
ammonia values. These are of interest as evidence that the ammonia forma-
tion of diabetic acidosis is due entirely to acid and not to any toxic perversion of
protein metabolism. On the other hand, the strict independence of coma and
acid intoxication is shown by the beginning of dialaetic coma, typical in every-
thing except hyperpnea, observed on two occasions (at admission and Sept. 9)
even with abnormally high plasma alkalinity. The effect of oatmeal on Sept. 9
is also remarkable, for it increased the ketonuria, raised the plasma bicarbonate
from 67.8 to 84.9 vol. per cent, and brought on prompt coma. Clinically,
therefore, it aggravated both the diabetes and the intoxication, irrespective of
chemical findings. It is interesting that such administration of carbohydrate
with reduction of fat should have had this effect, illustrating the fact that coma
is generally treated more safely and effectively with fasting than with carbo-
hydrate. The acidosis caused by oatmeal cleared up on fasting, and the urine
at death was free from both sugar and ferric chloride reactions. The relatively
low output of acetone bodies may be explained by the renal impermeability,
which doubtless favored retention. Neither qualitative nor quantitative tests
for acetone bodies in the blood were made, but the clinical picture indicated
that death was not due to acidosis.

Lipemia. — The blood at admission showed one of the most intense grades of
lipemia observed in this series. Analyses were not possible, and judgment is-
based on the thick, creamy appearance of the plasma. The lipemia showed no
perceptible diminution up to Sept. 9, but on Sept. 11, after transfusion on Sept.
10, the. plasma was perfectly clear. It was unfortunate that the effect of the
transfusion was not observed in this connection.

Levulose. — The patient had tolerated 3.3 gm. carbohydrate on Sept. 4. The
glucose tolerance in such a case must necessarily be close to zero. Nevertheless,
40 gm. levulose on Sept. 7 were assimilated without a trace of glycosuria. The
most remarkable feature was the clinical transformation wrought by the levu-
lose— a patient apparently dying restored in strength and consciousness within a
few hours. As saline h5T5odermoclysis had previously failed, this effect must be
attributed to the levulose and not to the fluid given with it. It is of interest
that the quantity of carbohydrate in the form of levulose was almost identical with
that given in oatmeal on Sept. 9. The contrast between the excellent assimi-
lation of levulose and the prompt glycosuria and ketonuria from oatmeal is
striking.

Transfusion. — This was performed for the purpose of improving strength, and
not with the idea of conveying any special substances curative of either the dia-
betes or the acidosis. The facts pertaining to this, as also other special features
of the case are given in Table XIII.

CASE RECORDS 363

The analyses of the father's blood immediately preceding the two transfusions
were as follows:

On Sept. 9, blood sugar 0.1 per cent, plasma sugar 0.091 per cent, corpuscle
sugar analyzed 0.125 per cent, calculated 0.114 per cent. Hemoglobin (Fleischl-
Miescher) 104 per cent. Corpuscles (hematocrit) 42 per cent. CO2 capacity of
plasma 56.4 per cent.

On Sept. 11, blood sugar 0.115 per cent, plasma sugar 0.137 per cent, corpuscle
sugar analyzed 0.097 per cent, calculated 0.083 per cent. Hemoglobin 95 per
cent. Corpuscles (hematocrit) 40 per cent. CO2 capacity of plasma 52.8 per
cent. The high sugar and low CO2 are explainable by the anxiety and haste of
the father when called to the hospital.

The purpose of improving strength was accomplished. No specific benefit to
the diabetic condition was perceptible from the transfusion, also there was no
indication of harm.

Sugar Permeability of Corpuscles. — As the abnormalities were so marked in
several respects, observations upon the sugar content of the corpuscles were made
in the same manner as with the exercise experiments in Chapter V; viz., by direct
analysis of the corpuscles after hard centrifugation, and by calculation from the
values for whole blood and plasma. The agreement between the two results is
generally as good here as can be expected. Deficient centrifugation, leaving
some plasma with the corpuscles, is probably responsible for the imduly high
figure from direct analysis on Sept. 1. No special abnormality in the permea-
bility of the corpuscles to sugar was shown under the conditions in question.

Remarks. — Obviously there was little real hope for such a patient under any
circumstances, and the relatives were surprised that life was continued for 10
days and that impirovement seemed to be evident at certain periods.

CASE NO. 46.

Male, married, age 48 yrs. Russian Jew; dry goods storekeeper. Admitted
Sept. 1, 1915.

Family History. — Mother died at 65 of supposed cardiac trouble. Father well
at age of 72. Only brother is well. Patient's wife and five children well, but
one daughter died of diabetes at age of 16, 9 years ago. No other heritable dis-
ease known in family.

Past History. — Healthy, rather sedentary Ufe without special strain or worry.
Pnemnonia at 10 years the only infection remembered. Diet has been the con-
centrated, monotonous type characteristic of his class. No special excesses.

Present Illness. — Patient distinctly remembers a day in Oct., 1914, when he
became acutely thirsty and drank much water. He immediately consulted a
physician, who reported 5.5 per cent sugar in the urine. On a diet of protein, fat,
and vegetables, glycosuria ceased in 2 days, and remained absent until Mar.,
1915, when rapid loss of weight also came on. From the normal 150 pounds he

364 CHAPTER ni

was now down to 130 pounds. He entered a hospital on May 5, 1915, where the
sugar and diacetic acid cleared up on fasting with brandy. These returned
within 2 days of his discharge from the hospital on May 17. His private physi-
cian, on account of fear of the diacetic acid present, then kept him on a liberal
carbohydrate diet. In July the condition was again cleared up in the hospital.
It returned promptly and was again treated with carbohydrate by the same
physician. Loss of weight and strength has proceeded rapidly. There is chronic
pain in back and legs.

Physical Examination. — Medium sized, thin, very exhausted appearing
patient. Skin dry. Eczema in axillas. Teeth in bad condition. Phar3Tix
reddened; tonsils not enlarged. Scattered lymph nodes palpable. Heart slightly
enlarged; systolic murmur heard all over precordia, loudest at apex. Slight
arteriosclerosis. Double inguinal hernia retained by truss. Knee jerks not
obtainable, even with reinforcement. Examination otherwise negative.

Treatment. — Fasting with whisky and 30 gm. sodium bicarbonate and 30 gm.
calcium carbonate daily was begim immediately. After Sept. S, both glycosuria
and ketonuria ceased. Alkali was stopped and whisky continued. Green
vegetables were then begun, and increased imtil glycosuria appeared with 140
gm. carbohydrate on Sept. 12. After a few days of low mixed ration, on Sept.
19 a diet was started containing 100 gm. protein and SO gm. carbohydrate.
Keeping this constant, the total calories were rapidly increased by addition of
fat, with the result that sugar and ferric chloride reactions returned in the period
Sept. 21 to 25. Exercise experiments were performed during this time as de-
scribed elsewhere (Chapter V). Exercise was then continued in the period Sept.
27 to Oct. 9. The result showed that the discontinuance of alcohol, combined
with muscular work to the point of exhaustion, did not cause acidosis as evi-
denced by either ferric chloride reactions or lowered plasma bicarbonate. Also,
though the total caloric ration was much higher than that which had brought
glycosuria on Sept. 21, sugar now remained absent until Oct. 6. A carbohydrate
tolerance test was next instituted in the usual manner. Glycosuria appeared
with an intake of 230 gm. on Oct. 30, but was not quite" continuous when the
intake was raised to 240 gm., or even to 300 gm. on Nov. 6. The heavy exercise
probably contributed somewhat to this tolerance. The patient was discharged
on Nov. 16 and resumed business, feeling well.

Acidosis. — Moderate acidosis was indicated by the heavy ferric chloride reac-
tion, 1.1 gm. ammonia nitrogen, and plasma bicarbonate of 41.9 vol. per cent at
admission. Under fasting and alkali the ammonia quickly fell to normal, and
the CO2 capacity rose to the high level of 73 per cent. The ferric chloride reac-
tion diminished even during alkali administration, and became negative the day
after alkali was stopped. But within 2 days thereafter (Sept. 7), the CO2 ca-
pacity had fallen to 50.4 per cent. The lower figure of 39 per cent on Sept. 8
was obtained after hard exercise. Other tests in exercise experiments are omitted
from the graphic chart. The last determination, on Oct. 27, during the carbo-

CASE RECORDS 365

hydrate period, showed a low normal figure of 55.8 per cent. The ferric chloride
reactions behaved as frequently noted, coming and going about the same time
with small traces of glycosuria.

Blood Sugar. — On the first day in hospital the sugar in whole blood was 0.555
per cent, in plasma 0.606 per cent. Fasting brought a very quick fall, but not
to normal, and marked hyperglycemia returned on feeding. The renal threshold
was probably high. On Sept. 25, the percentage in plasma was 0.371 per cent
as against 0.244 per cent in whole blood, indicating a very low sugar content in
the corpuscles. The low plasma sugar of 0.123 per cent on Sept. 29 was obtained
immediately upon finishing noon lunch, the patient having spent the morning
at heavy exercise. The tendency of the blood sugar was continuously downward,
the last analyses, on the morning of Nov. 13, showing 0.113 per cent in whole
blood and 0.145 per cent in plasma.

Weight and Nutrition. — Weight at admission 51 kg.; at discharge 47.4 kg., a
reduction of 3.6 kg. The patient had been pale and badly exhausted at admis-
sion. He was accepted because he appeared to represent a very pronounced
degree of lowered resistance and susceptibility to infectious and other accidents.
On imdernutrition treatment he gained strength decidedly with the combination
. of loss of weight and heavy exercise, and though thin, pronounced himself feeling
well. The diet prescribed at discharge was 100 gm. protein, 50 gm. carbohydrate,
and 2000 calories (about 2.1 gm. protein and 42 calories per kg., reduced by the
weekly fast-days to 1.8 gm. protein and 36 calories per kg.). Three factors were
considered here: first, the low weight upon which this reckoning is based (47.4
kg. as against 65 kg. normal); second, the hard exercise prescribed; and third, the
steady improvement, justifying some slight liberality of diet, which also seemed
desirable for the purpose of building up weight and strength.

Lipemia. — The plasma at admission was heavily lipemic. This Upemia was
present in marked degree up to Sept. 3, then ceased rather abruptly, for the plasma
on Sept. 4 was clear. No analyses were done.

Subsequent History. — The condition remained favorable, and glycosuria was
absent except for a trace on Feb. 1. About Feb. 20, he contracted a severe cold,
and shortly thereafter began to raise large amounts of foul smeUing sputum.
When seen on Mar. 4 he was a very sick man. Necrotic tissue but no tubercle
bacilli were found in the sputum. Glycosuria and acidosis had returned with
this infection. The patient was referred to another hospital, and died of pul-
monary gangrene on Mar. 15, 1916.

Remarks. — The low resistance suspected at admission was confirmed by the
outcome. Diabetes probably contributed to increase susceptibility, but it is
believed that the treatment, by improving strength and permitting outdoor
exercise, tended to raise rather than lower resistance in such a case.

366 CHAPTER m

CASE NO. 47.

Female, married, age 31 yrs. American; houseworker and canvasser. Ad-
mitted Oct. 6, 1915.

Family History. — Parents alive; Bright's disease suspected in father. Two
sisters are well. Maternal grandmother died of tuberculosis. Husband healthy.
Patient pregnant only once; the child is well, aged 8. History otherwise negative.

Past History.— Liie was spent in Wisconsm until 11 years ago, then in Porto
Rico until 1 year ago, since then she has lived near New York. Always strong and
healthy. Has had only some mild childhood diseases. Never nervous. Habits
and diet normal.

Present Illness. — This began 4 years ago with pruritus vulvae, not relieved by
local treatments, but increasing during a year. By the end of the year poly-
phagia, polydipsia, and polyuria were present, and the normal weight of 185
poimds had fallen to 145. A physician then diagnosed diabetes and merely for-
bade sugar and starch. The pruritus has remained continuously present, and
glycosuria was never reduced below 2 per cent. The patient applied to the In-
stitute because she had been informed that she could not live more than 3 months.

Physical Examination. — Height 170.1 cm. A tall, large boned woman without
marked emaciation but with flabby skin and muscles. She appears strong and
phlegmatic by nature, but worried and upset at present. Cheeks, high color;
no dyspnea or other acute symptoms. Teeth in fair condition. Tonsils slightly
enlarged. Lymph nodes palpable only in axillse. Reflexes normal. Superficial
genital infection from scratching. Blood pressure 90 systolic, 60 diastolic. Ex-
amination otherwise negative.

Treatment. — The patient was placed on an observation diet of 100 gm. pro-
tein, 100 gm. carbohydrate, and 3000 calories. Heavy glycosuria continued and
acidosis increased. After 3 days of this diet a high ammonia and low plasma
bicarbonate indicated danger. Accordingly 2 days of plain fasting were given
(coffee and soup, each 300 cc.) followed by 4 days with alcohol up to 600 calories.
Glycosuria was absent after Oct. 12, but the fasting was continued for 3 days
longer, because it was acting favorably upon the acidosis and the patient was
of a type requiring sharp undernutrition. With the cessation of glycosuria, the
distressing vaginal pruritus of 4 years duration promptly cleared up. A carbo-
hydrate test was then instituted. The ferric chloride reaction thus disappeared,
and the limit of tolerance was foimd to be 240 gm. carbohydrate. After a fast-
day on Nov. 14, the diet on Nov. 15 and 16 was 100 gm. protein and 2000 calories
without carbohydrate. In order to test the effect of fat, this diet was built up
by addition of fat. The first trace of ferric chloride reaction appeared with
2500 calories on Nov. 20. This reaction increased, the blood sugar rose, and
glycosuria appeared on Nov. 27 with 4000 calories. It showed the characteris-
tics of fat glycosuria in being slight and stubborn, not increased by the rise to
4500 calories on Nov. 29 and 30. Protein and fat were then stopped and nothing

CASE RECORDS 367

but green vegetables given, increasing from 10 gm. carbohydrate on Dec 1 to
70 gm. carbohydrate on Dec. 4 The ferric chloride reaction promptly cleared up,
but traces of glycosuria persisted. After the fast-day of Dec. 5, a diet of 100 gm.
protein and 2000 calories was begun, as on Nov. IS and 16, but with the addi-
tion of first 10 and then 20 gm. carbohydrate. After Dec. 9 both glycosuria and
ketonuria were absent on this diet, and on Dec. 18 it was possible to increase the
carbohydrate to 70 gm. without glycosuria. The effect of the fat in lowering toler-
ance is thus eVident. The patient was discharged Dec. 22 on a diet of 100 gm.
protein, SO gm. carbohydrate, and 2000 calories, (1.6 gm. protein and 31.8 cal-
ories per kg., reduced by the weekly fast-days to 1.4 gm. protein and 27.3 calories
per kg.).

Acidosis. — The attending physician sent this patient to the Institute because
confronted with the dilemma formerly feared; i.e., continuous glycosuria not-
withstanding restriction of carbohydrate, and acidosis present even with carbo-
hydrate in the diet. The rise of ammonia nitrogen from 1.62 gm. on Oct. 7 to
3.63 gm. on Oct. 10 probably indicates that 10 gm. carbohydrate represented
greater restriction than this patient had been accustomed to. The CO2 capacity
of the plasma, 41 per cent on Oct. 10, also gave evidence of well marked acidosis
on this diet. There was the usual improvement on fasting, the CO2 capacity
rising promptly without the use of alkali, but not attaining the normal hmit
until near the close of the carbohydrate test on Nov. 12. Protein-fat diet there-
after brought a fall, and particularly with the increase in fat it is seen that well
marked acidosis developed, the CO2 capacity of 39 per cent on Nov. 27 being
lower than recorded even in the first days after admission. Coma would almost
certainly have resulted from continuance of such an experiment. The fast-day
of Nov. 28 gave a prompt respite, so that the CO2 capacity on the morning of
Nov. 29 had risen steeply to almost S3 per cent. On the morning of Nov. 1,
after 2 more days of higher fat intake, it showed a drop, but the small quantities
of carbohydrate and omission of fat brought it up promptly within normal limits
by Dec. 2. Thereafter, with reduced fat and introduction of a little carbohy-
drate, fully normal values of blood bicarbonate were obtained.

Ammonia determinations had been discontinued on Oct. 12, after it was evi-
dent that the course was downward. It may be assumed that the curve fell to
normal during the carbohydrate test. Following the fat experiment it was up
to 2.24 gm. N on Nov. 1. There was a prompt drop with carbohydrate, followed
by a rise to 1.92 gm. N on the lower fat intake, and another fall after the fast-
day of Dec. 12. The ferric chloride reaction roughly corresponded to the other
evidences of acidosis.

Blood Sugar. — Though the restriction of carbohydrate caused acidosis, the
high values of 0.38 per cent sugar in whole blood and 0.S24 per cent in plasma
on Oct. 9 indicated how far the diet stUl exceeded the tolerance. With fasting
there was a prompt fall in blood sugar, but not to normal. H}rperglycemia
gradually increased during the carbohydrate test, and persisted after it to Nov.

368 CHAPTER ni

17. The abstinence from carbohydrate showed its effect in a fall on Nov. 20; but
an increase of blood sugar due to an increase of fat in the diet was then clearly
demonstrable, leading to glycosuria as mentioned. After the undernutrition
period (Dec. 1 to 5), the first normal plasma sugar was obtained on Dec. 6.
Thereafter the restriction of fat, though protein was kept the same and carbohy-
drate was added, resulted in a fall of blood sugar so that the patient was dis-
missed with a normal plasma sugar of 0.12 per cent.

Weight and Nutrition. — The weight at admission was 67.3 kg!, at discharge
62.9 kg. The treatment thus represented undernutrition to the extent of 4.4 kg.
At the same time vigorous exercise was employed. The patient was naturally
strong, and after her immediate distress was relieved she was soon able to walk
4 miles, climb 40 flights of stairs, and practice roller skating and other exer-
cises daily. Her weight at discharge was satisfactory for both strength and
looks. Her muscles were firm, and she was in splendid health subjectively and
objectively.

Subsequent History. — The patient reported on Jan. 4 free from glycosuria, but
weighing 64.9 kg., a gain indicating that she had not been faithful to the prescribed
exercise and quantity of diet. She was instructed to bring the weight down to that
at discharge. Notwithstanding warnings, she gradually became more careless in
regard to diet, and ceased weighing food. Glycosuria returned first in occa-
sional traces which were cleared up, and then during Apr. continuously. On
May 24, she was still looking perfectly well, but complained of weakness and
weariness along with glycosuria. The sugar in both whole blood and plasma
was 0.201 per cent, CO2 capacity 52.1 per cent. When seen again on July 22,
the findings were heavy glycosviria, moderate ferric chloride reaction, blood sugar
0.370 per cent, plasma sugar 0.385 per cent, CO2 capacity 56 per cent, weight
68.3 kg. She was not seen again imtU Jime 7, 1917, when her weight was 70
kg., due in considerable part to edema. She was still looking and feeling fairly
well, but the urine showed a heavy sugar and slight ferric chloride reaction. The
carelessness ia diet was continuous. Downward progress clinically, which seemed
to be slow in appearing, was very rapid at the close, and reports in July, 1917
indicated that the patient was close to death from weakness and acidosis.

Remarks. — The case would have been a diflncult one to manage under former
treatment, but with the present methods showed itself as only moderately severe.
The complete clearing up of the condition both chertiicaUy and clinically served
to prolong comfort, strength, and Ufe, even though diet was violated afterwards.
The patient lacked the necessary wiU power to adhere to diet, and downward
progress was therefore inevitable. She gained strength as she lost weight in hos-
pital, and lost strength as she gained weight outside the hospital. At no time
could it be said that she was stronger or better ofiE on a diet in excess of the
tolerance.

CASE RECORDS 369

CASE NO. 48.

Male, unmarried, age 20 yrs. American; shipping clerk. Admitted Oct. 7,
1915.

Family History. — Partly unknown. Two uncles died of tuberculosis. Family
said to be free of diabetes, cancer, syphilis, and nervous troubles.

Past History. — ^Healthy life in rather poor surroundings. Childhood diseases
unknown. Occasional mild sore throats. Considerable trouble with teeth. No
venereal disease. Reached graduating class in grammar school at 15, then began
work as delivery boy, and 6 months ago was promoted to shipping clerk. No
alcoholism. Cigarettes smoked to excess. Has had more than the average
appetite for candy, pastry, and sweet things.

Present Illness. — Polyphagia, polydipsia, and polyuria began 1 year ago. Diag-
nosis was made within a month, and the physician forbade sugar and starch and
ordered a teaspoonfid of sodium bicarbonate three times a day. Patient did not
adhere to the diet and became worse. Later he was treated by another physician
and at a hospital clinic, and at the latter place was advised to come to this
Institute.

Physical Examination. — A round shouldered, narrow chested, underdeveloped,
imdernourished boy. Teeth in fair repair; tonsils normal. General examination
negative.

Treatment. — (No graphic chart.) The usual heavy glycosuria and ketonuria
were present, but no signs of immediate danger. After 3 days of observation
diet, a S day fast cleared up the glycosuria. Green vegetables were begun on
Oct. 15, and 10 gm. carbohydrate added daily, until persistent traces of glycosuria
appeared with 130 gm., Oct. 27 to 30. Meanwhile the ferric chloride reaction
became negative. A mixed diet was then rather rapidly built up, but though this
was adequate in amount, the patient proved himself entirely imtrustworthy.
He was kept in the hospital vmtil July 28, 1916, but always showed the undepend-
able character and degeneracy of the excessive cigarette smoker, and continually
broke rules in regard to both diet and smoking. He insisted that he must have
sugar on occasions, and 40 to SO cigarettes daily. Under hospital management
he had been kept free from glycosuria nearly the entire time. He was discharged
with the certainty that he would go rapidly downhill.

CASE NO. 49.

Female, divorced, age 30 yrs. American; seamstress. Admitted Oct. 9,
1915.

Family History. — Father died of peritonitis, following gall stones. Mother
living, aged 55, also has gall stones. Four brothers died in infancy; one brother
and one sister are well. No diabetes or other heritable disease in family.

Past History. — Measles, mumps, chicken-pox, scarlet fever, before 10. Mem-
branous croup at 6 years requiring intubation. Many sore throats, espyecially

370 CHAPTER ni

tonsillitis previous winter. Married 8 years ago. Two children 13 months
apart; both high forceps and died of weakness or convulsions within 6 months.
Patient always nervous and overexcitable. 6 years ago nervous breakdown
confined her to bed for 12 weeks. No excesses in diet or otherwise.

Present Illness.— Shortly before Christmas, 1914, began polyphagia, polydipsia,
and polyuria. She found she had lost 25 pounds weight smce the previous sum-
mer. She was given the usual diet but did not adhere closely to it. Last win-
ter vision became blurred; glasses have helped somewhat, but at present she can-
not read and has difficulty walking about because of blurring of sight. Has
been tired and weak for 6 months past, and sleeps a couple of extra hours in the
afternoon.

Physical Examination. — Patient fairly developed, only slightly emaciated.
Mouth and throat normal. No lymph node enlargements. Reflexes normal.
General examination negative.

Treatment. — The patient was admitted at 11 a.m., and up to 6 a.m. the next
morning excreted 118 gm. glucose, with a heavy ferric chloride reaction and 2.93 gm.
ammonia nitrogen. The first CO2 determination on Oct. 9 was 34.4 per cent.
The diet on Oct. 9 was 100 gm. protein, 100 gm. carbohydrate, and 2200 calories.
The ammonia nitrogen rose to 3.36 gm., and the CO2 capacity on the morning of
Oct. 10 was down to 27.8 per cent. The patient was drowsy, with face flushed,
and spent most of her time in seemingly normal sleep. There was no marked
dyspnea, but the coryza present at admission persisted, with temperature up to
100.5° F. On Oct. 10 fasting was begun, with 120 cc. whisky and 60 gm. sodium
bicarbonate. Whisky was continued, but no more alkali was given. The CO2
capacity rose and the ammonia fell, and acidosis symptoms cleared up. Glyco-
suria ceased after 5 days of fasting. 10 gm. carbohydrate in green vegetables
were added to the whisky on Oct. 15. Whisky was then discontinued and carbo-
hydrate continued at 30 gm. daily. This caused glycosuria, which cleared up
under exercise as noted below. It was then possible to make the usual increase
of 10 gm. carbohydrate daily. A trace of glycosuria appeared with 150 gm.
carbohydrate on Nov. 2, then disappeared, and reappeared with 170 gm. carbo-
hydrate on Nov. 5. Meanwhile the ferric chloride reaction cleared up. A diet
of 2000 calories with 75 gm. protein and 15 gm. carbohydrate was then begun
with the usual weekly fast-days. The attempt to increase carbohydrate to 40
gm. on Nov. 23 resulted in glycosuria. The patient was dismissed on Dec. 3
feeling strong and well, having recovered her vision perfectly. An oculist found
vision normal and considered that the blurring had been a functional weakness
of accommodation.

Acidosis. — Even though the diet on Oct. 9 contained 100 gm. carbohydrate,
restriction to this extent brought on symptoms of impending coma. There was
the usual clearing up on fasting, and the recovery of a considerable carbohydrate
tolerance. It is noteworthy that mixed diet tended to bring back the ferric
chloride reaction. In the last analyses on Dec. 1, preceding discharge, the CO2

CASE RECORDS 371

capacity of the plasma was normal and the ferric chloride reaction negative, but
a slight acidosis was indicated by the ammonia nitrogen of 1.24 gm. The sugar
in both whole blood and plasma at admission was 0.333 per cent. On Oct. 15,
after 2 days freedom from glycosuria, the sugar was still 0.217 per cent m whole
blood and 0.244 per cent in plasma. Notwithstanding the high carbohydrate in-
take, the blood sugar on Nov. 4 was down to 0.169 per cent, plasma sugar 0.164
per cent, in consequence of continued undernutrition and exercise. After a rise
to 0.204 per cent on Nov. 11 with mixed diet, the tendency of the blood sugar was
downward, and on Dec. 1 it was 0.133 per cent in whole blood, 0.167 per cent
in plasma.

£«ercMe.^Glycosuria had appeared with green vegetables representing 30
gm. carbohydrate on Oct. 17, and persisted with this intake on the following
days. Beginning Oct. 19, exercise was ordered. The patient skipped rope for
IS mmutes daily, and on Oct. 19 climbed 32 flights of stairs, on the 20th 48 flights,
on the 21st 96 flights. On this day glycosuria ceased. Exercise to the point of
exhaustion was continued as carbohydrate was increased on the following days.
The effect in raising tolerance was demonstrated by the cessation of glycosuria
as described, and the exercise doubtless contributed toward the high tolerance
then displayed. Nevertheless simple continuance of undernutrition represented
in the carbohydrate period must be given credit as the most beneficial factor.

Weight and Nutrition. — ^The weight at entrance was 52.4 kg., at discharge 49.8
kg., the treatment thus representing undernutrition to the extent of 2.4 kg. The
diet at discharge was 75 gm. protein, 25 gm. carbohydrate, and 2000 calories,
representing approximately 1.5 gm. protein and 40 calories, reduced by the weekly
fast-days to an average of about 1.3 gm. protein and 34 calories per kg. This
was considered a low diet in view of the amount of exercise which the patient was
ordered to continue at home. She was some 36 pounds below her normal weight
and was not expected to gain weight on this ration. Faith was largely reposed in
exercise to bring down the blood sugar further and raise the tolerance. Later
knowledge makes it evident that a lower diet with less strenuous exercise would
have been better treatment, and reduction of the too large fat intake would
have been the best means of bringing down both the ammonia and the blood
sugar.

Subsequent History. — In Jan., 1916, the patient showed traces of glycosuria dur-
ing a short attack of grippe. Thereafter she was free from sugar and ferric
chloride reactions up to the last report in Feb. The next word received was
notice of her death on May 19, 1916. Inquiry elicited the fact that she had
broken diet about 1 month before death, and died with symptoms of diabetic
coma.

Remarks. — The progress to a fatal end in 1 month indicates the severity of the
case, and this result of breaking diet is in contrast to the excellent condition at
the time of discharge.

372 CHAPTER m

CASE NO. 50.

Widow, age 54 yrs. American; teacher. Admitted Oct. 8, 1915.

Family History. — Negative for diabetes or other heritable disease.

Past History. — Very healthy life. No illnesses beyond those of childhood.
Never pregnant. Regular habits. No excesses. Appetite, digestion, bowels,
and menstruation normal until present illness; no menstruation since.

Present Illness. — In 1907, the patient entered a sanitarium on account of a
"nervous breakdown." This had begim so gradually that the exact onset was
unknown. She complained of general weakness and loss of energy, memory, and
mental powers, also her teeth and hair were falling out, speech was slow, tongue
thick, and face swollen. The diagnosis of myxedema was made, and thyroid ex-
tract restored apparently normal health. In 1912 she returned to the sanitarium,
having taken thyroid extract throughout the interval. This time she had poly-
phagia, polydipsia, and pol)airia. The diagnosis of diabetes was made, and
thyroid extract was ordered discontinued for fear it might aggravate the dia-
betes. She has been unable to get along without thyroid, and has therefore con-
tinued to take it at intervals as the myxedema S3Tnptoms returned. Loss of
weight has been only moderate, and the chief symptoms are a general breakdown,
with weakness and nervousness, along with marked myxedema S)rmptoms as
above mentioned, coryza, headache, and complaint of pains all over the body.

Physical Examination. — Height 152.2 cm. A well developed, well nourished
woman; hair turning gray, slightly coarse, abundant; broad puflEy face; dry skin;
pasty color; eyebrows and lashes scanty. A number of teeth missing; the others
show some caries and pyorrhea. Throat normal. Lobes but not isthmus of
thyroid palpable, apparently normal in size and consistency. Heart and Ivmgs
negative. Liver edge palpable O.S cm. below costal margin. Blood pressure 90
systolic, 75 diastolic. Fingers short, thick, not clubbed. Reflexes normal. The
patient appeared as if intoxicated, and speech was difficult, almost incoherent.
The diagnosis of myxedema was confirmed by several observers, and it was con-
sidered possible that intoxication of acidosis character was also present, not-
withstanding the low ammonia and high CO2.

Treatment. — On Oct. 8 the diet contained 64 gm. protein, 28 gm. carbohydrate,
and 1500 calories. The next day, with diminishing appetite, it was 35.5 gm. pro-
tein, 38 gm. carbohydrate, and 1375 calories. On this day there was nausea and
one attack of vomiting. The symptoms at admission were still present. The
highest temperature was 100.2° F. Fasting was begun on Oct. 10, with 300 cc.
clear soup daily. 30 cc. castor oil and several high colon irrigations removed
large quantities of feces. Glycosuria cleared up after 48 hours. On Oct. 10, 6
gm., and on Oct. 11, 22 gm. sodium bicarbonate were given. The urine re-
mained acid or neutral, and the ferric chloride reaction, which had been slight,
was increased to only moderate degree. On Oct. 13, 10 gm. carbohydrate in the
form of green vegetables were given, and increased on subsequent days until on

CASE RECORDS 373

Oct. 26, 110 gm. were taken without glycosuria, and a fast-day was necessary the
next day because of indigestion due to the quantity of vegetables. The ferric
chloride reaction had cleared up, and weakness and other symptoms had greatly
improved. After the fast-day exercise was begun, particularly with a view to
improving digestion, and by Nov. 1 the patient was on a regular program of
walking 10 blocks and 24 flights of stairs daily. The bulk of vegetables was
diminished by giving potato. On Nov. 2, the patient, feeling well and cheerful,
experienced the sensation that the left foot was asleep. She stamped it and fell,
fracturing the tip of the fibula. The leg was put up in plaster and exercise neces-
sarily stopped. From Nov. 5 to 13, 200 gnl. carbohydrate daily were tolerated
without glycosuria and with diminishing blood sugar. Beginning Nov. IS, a
mixed diet of 2000 calories and 65 gm. protein was begun with high carbohydrate,
for purposes of a test with thyroid extract as described below. The subsequent
glycosuria was cleared up by the fast-days of Dec. 19 and 20, after which a diet
was bmlt up of 75 gm. protein and 1500 calories, with carbohydrate graduaUy
increasing up to 90 gm. on Jan. 14. The cast was removed from the fractured
leg on Dec. 8, repair having been uneventful and perfect. She was discharged
Jan. 14, 1916, with the feeling and appearance of complete health, to resume her
duties as teacher.

Acidosis. — On the chemical side this never amounted to more than a slight
ferric chloride reaction, but there was prompt and striking improvement in the
intoxication symptoms under the usual treatment for acidosis. One subsequent
feature is the steady rise of the CO2 curve with increasing carbohydrate intake
up to the very high value of 74.6 per cent on Dec. 17, then, with carbohydrate
almost excluded, the steep fall to 53.8 per cent on Dec. 30. By Jan. 5, it had
risen within low normal limits, without the aid of alkali, perhaps with the aid of
the small quantity of carbohydrate.

Blood Sugar. — At admission, sugar was 0.375 per cent in whole blood and 0.371
per cent in plasma. By Oct. 16, it was found normal (0.113 per cent). With
the subsequent high carbohydrate intake it tended to rise, but was brought
promptly to normal on the morning after the single fast-day of Oct. 27. Values
0.3 to 0.32 per cent were obtained on Nov. 1 and 3 durmg digestion without gly-
cosuria, but those taken mornings before breakfast tended to fall, so that toward
the close of the period in hospital normal figures were the rule.

Weight and Nutrition. — The weight at entrance was 49.6 kg., at discharge 46.2
kg., the period of treatment thus representing imdernutrition to the extent of
3.4 kg. The long period of relative protein abstinence is noteworthy, inamuch
as from Oct. 10 to Nov. 14 the patient received nothing but green vegetables, the
protein of which is low in quantity and poorly assimilable. During this period
there was a striking gain instead of loss of strength, and a fractured bone healed
rapidly. The diet prescribed at discharge was 75 gm. protein, 50 gm. carbohy-
drate, and 1500 calories, representing, at her reduced weight, approximately 1.63
gm. protein and 32 calories per kg., diminished by the weekly fast-days to 1.4
gm. protein and 28 calories per kg. This was as much as her appetite desired.

374 CHAPTER ni

Thyroid.— The history is remarkable in that diabetes accompanied not hyper-
thyroidism, but typical myxedema. Another surprising feature was that
with the usual diabetic treatment of fasting followed by green vegetable diet,
without thyroid or other medication, the myxedema symptoms rapidly improved,
the mind and speech became clear, the face lost its puffy appearance, and the
patient looked and felt ahnost well. It is not known whether this indicates that
fasting may be beneficial for myxedema uncomplicated by diabetes. It might be
supposed that the prolonged treatment with thyroid extract had brought on the
diabetes. It was desirable to test this possibility, and also to estabUsh the place
of thyroid extract in the treatment- of this patient. Accordingly on Nov. IS, a
purposely high diet was begun, containing 65 gm. protein, ISO gm. carbohydrate,
and 2000 calories. Glycosuria appeared on Nov. 17 but ceased the next day. On
Nov. 19 the carbohydrate was increased to 2S0 gm. and at the same time 0.45
gm. desiccated thyroid was given, increased to 0.9 gm. the next day with the
same diet. Glycosuria was heavy on the 19th, but cleared .up completely on the
20th. After the routine fast-day on the 21st, the same diet was continued without
thyroid. There was glycosuria on Nov. 23, a trace on the 26th, and continuous
well marked reactions from Nov. 28 to Dec. 6. It thus appeared that the thyroid
feeding had not injured the tolerance and perhaps had been slightly beneficial.
Beginning Dec. 2 the carbohydrate was increased to 350 gm., with resulting con-
tinuous glycosuria. On Dec. 6, 0.032 gm. desiccated thyroid was given, the
same on the 7th, 0.064 gm. on the 8th and 9th, 0.128 gm. on the 10th, and so
on increasing up to 0.32 gm. on Dec. 18. Glycosuria stopped abruptly on the
first day after beginning thyroid, and remained absent on the small doses for 3
days, whUe the blood sugar also fell to normal. Thereafter, with increasing
th3n:oid dosage, glycosuria returned and became heavier, finally requiring 2 fast-
days to stop it. Thyroid was omitted after Dec. 18, and by the first week in
Jan. slight impairment of energy and mentality had returned. Therefore during
the last week in hospital 0.05 gm. thyroid was given daUy and was ordered con-
tinued after discharge. On this she was free from symptoms of thyroid deficiency.
The tests, as far as judgment is possible, indicated that the carbohydrate toler-
ance was slightly improved by small doses of thyroid, although larger doses might
injure it.

Subsequent History. — The patient continued well, and voluntarily diminished
her diet because it was more than she desired. She twice experiinented with
herself, taking chocolate cake once and bread once, with immediate glycosuria
which cleared up promptly. Otherwise she remained free from glycosuria and
other symptoms. Apr. IS, sugar in whole blood was 0.142 per cent, in plasma
0.147 per cent. By July 11, the weight had fallen to 44.2 kg.; blood sugar was
0.137 per cent, plasma sugar 0.141 per cent, CO2 capacity 52.3 per cent. The
patient continued her duties as teacher and kept up thyroid medication as indi-
cated by her own feelings. She began to take small quantities of bread without
glycosuria. She was readmitted Oct. 2, 1916, at her own request to learn if these
were safe.

CASE EECOBDS 375

Secmd Admission.— Oct. 2, 1916. Patient well nourished physically and
mentally vigorous; no appearance of myxedema. General examination normal.
Blood pressure 110 systolic, 78 diastolic. She was found to remain free from
symptoms on the prescribed diet with SO gm. carbohydrate taken in the form
of bread and fruit. The blood sugar in daily determmations ranged from 0.102
to 0.118 per cent. As the patient was satisfied with the diet, it was decided to
let it remain as stated. She was discharged Oct. 8, 1916, and has since contin-
ued her work in good health.

CASE NO. 51.

Male, age 7 yrs. Polish American; schoolboy. Admitted Oct. 10, 1915.

Family History.— Farents are Polish immigrants, well, except that mother is
somewhat nervous. Only sister is well. No diabetes or other heritable disease
known in family.

Past History. — Healthy life in small New York town. Whooping-cough the
only illness known. Ordinary habits, diet, and development.

Present Illness. — 1 year before admission patient was seen by a physician in
his home town, with weakness and coma such that another physician had refused
the case. The history was of polyuria and rapid loss of flesh and strength for
only a week or two before that time. Intense glycosuria and acidosis were pres-
ent. The patient recovered from the coma and has been kept almost contihuously
sugar-free by the local physician under fasting treatment. It became increasingly
difficult to maintain freedom from glycosuria, and the patient was therefore re-
ferred to the Institute.

Physical Examination. — Height 121.1 cm. A well developed, pale boy with
apparently moderate loss of weight. General examination normal. No acute
symptoms.

Treatment. Only moderate sugar and ferric chloride reactions were present at
admission. The former became negative on an observation diet of 40 gm. pro-
tein, 10 gm. carbohydrate, and 1000 calories. The latter was also negative after
a single fast-day on Oct. 16. A carbohydrate test was then instituted in the
usual manner, and glycosuria appeared with 100 gm. carbohydrate (Oct. 26 to
30). Mixed diet was then begun, with the usual weekly fast-days. Traces of
glycosuria indicated that 50 gm. carbohydrate were too high. In general, a
diet of 40 gm. protein, 25 gm. carbohydrate, and 1100 calories, with routine weekly
fast-days, was tolerated with normal urine. He was discharged on this diet
Jan. 19, 1916, with the appearance of very satisfactory health and strength.

Acidosis. — ^Although the ferric chloride reaction was never more than moder-
ate, the first CO2 determination on Oct. 16, following a protein-fat diet with 10
gm. or less of carbohydrate, showed the rather low value of 44.8 per cent. During
the carbohydrate test this rose to 59 per cent by Oct. 29. The fast-day of Oct.
31 brought a remarkable drop in both the sugar and bicarbonate of the blood,
the CO2 capacity on the following morning being down to 33 per cent. On the

376 CHAPTER m

ensuing mixed diet it promptly rose, without the aid of alkali, and after a moder-
atfely subnormal period up to Nov. 18, thereafter held a normal level for a child.
On Jan. IS, shortly before discharge, it was 57.2 per cent. The ammonia output
in the few determinations made was normal.

Blood Sugar. — The first analysis on Oct 25, during the carbohydrate test,
showed 0.35 per cent sugar in whole blood and 0.37 per cent in plasma without
glycosuria, indicating a high renal threshold. With glycosuria present on Oct.
29, the sugar during carbohydrate digestion was at the high level of 0.46 per cent
in whole blood and 0.511 per cent in plasma; but on the morning of Nov. 1, after
the preceding fast-day, it was down to the normal level of 0.109 per cent. Hyper-
glycemia then ensued on mixed diet, but by Nov. 11 the percentage was below
0.1 in both whole blood and plasma. Thereafter the tendency of the curve was
toward normal; but the rise to 0.164 per cent on Jan. 15, shortly before dis-
charge, was an unfavorable indication, which should have called for more stringent
treatment.

Weight and Nutrition. — The weight at admission was 18.3 kg.; at discharge 17
kg. Therefore, instead of growth, the undernutrition resulted in a loss of 1.3 kg.
in a little over 3 months. The diet at discharge represented approximately 2.3
gm. protein and 65 calories per kg., diminished by the weekly fast-days to about
2 gm. protein and 56 calories per kg. The boy had been on nearly or quite such
a diet thoughout most of the hospital period, and it would seem that a normal
child might have gained weight under these conditions. Part of the explanation
is found in exercise, for he was kept busy with vigorous games and gymnastics
all day long. The exercise was beneficial from the standpoint of enjoyment,
freedom from nervousness, and development of strength and general health, but
it is evident that the tolerance was not raised very high.

Subsequent History. — The patient attended school, j)layed, and remained well,
with no glycosuria except during a brief cold in Mar. In May, glycosuria began
to appear frequently, and the explanation proved to be that the boy was taking
extra food unknown to his parents. Because of inability to overcome this difii-
culty, the patient was readmitted June 27, 1916.

Second Admission. — The weight was 18 kg.; i. e., a gain of 1 kg. since discharge.
There was no detectable gain in height. Moderate sugar and ferric chloride
reactions were present up to July 1, on observation diets of 40 gm. protein, IS
gm. carbohydrate, and 1000 calories daily, but diminishing during this time, in-
dicating that the trouble had lain in violations of diet during the 2 months pre-
ceding. On July 2, the remaining sugar and diacetic reactions were cleared up
by a single fast-day. 1 more fast-day was given, then green vegetables were
begun in the usual manner, with addition of 10 gm. carbohydrate daily, and gly-
cosuria appeared with 40 gm. carbohydrate on July 7 and 8, indicating a decided
loss of tolerance as compared with the 100 gm. at the former admission. Mixed
diet was then built up in the usual manner, and then kept at 30 to 35 gm. pro-
tein, 5 to 10 gm. carbohydrate, and 700 calories. The patient was disharged on
this, Aug. 17, 1916. The weight had been approxunately 17 kg. throughout this

CASE RECORDS 377

time. The diet thus represented approximately 2 gm. protein and 41 calories
per kg., diminished to about 1.7 gm. protein and 35 calories by the weekly fast-
days. In correspondence with the other conditions, the patient was not so strong
and well as before; he was still active, and comfortable except for the narrow
diet, but perceptibly below normal in flesh, figure, and spirits.

Subsequent History. — The patient again deceived his parents in regard to diet
and showed sugar more and more. Death occurred Oct. 11, 1916; details were
not obtained.

Remarks. — The essential cause of trouble lay in the home conditions of an
uneducated Polish laboring family. Aside from this, the following two features
are ijoteworthy. First, there was the inabiUty to grow normally, possibly char-
acteristic of severe diabetes in some children even when the diet is adequate.
Simple undernutrition should scarcely have prevented gain in stature. Second,
no obvious recuperation or repair of the assimilative function was displayed
by this child under these circumstances. In the absence of any marked tendency
to gain tolerance, and under the policy of maintaining the highest possible strength
and nutrition, which is now known to be a mistake, downward progress must
inevitably have occurred later, even if the patient had been faithful to the pre-
scribed diet.

CASE NO. 52.

Female, unmarried, age 27 yrs. American. Admitted Oct. IS, 1915.

Family History. — Negative for diabetes or other heritable disease.

Past History. — Healthy life under excellent hygienic conditions in a southern
state; Measles and chicken-pox in childhood. Habits regular; no dietary ex-
cesses or overindulgence in sweets.

Present Illness. — Began with general lassitude in 1911. Medical examination
showed nothing but a slight glycosuria. A physician prescribed a diet with
carbohydrate limited to one slice of toast and one baked potato daily. There
were no regular urine examinations for the next 2 years. Occasional tests showed
sugar sometimes present, sometimes absent. During the past 2 years glycosuria
has been continuous. The patient had no special thought of danger, and con-
tinued to lead her ordinary life and to feel fairly well. In May, 1915, she began
to lose weight appreciably, and was treated by the same physician with fasting
in hospital. Glycosuria ceased with 5 days of continuous fasting. She then toler-
ated a hberal diet without glycosuria, but a relapse occurred after her return
home, and her physician advised coming to this Institute. Menstruation was
absent 4 months prior to admission.

Physical Examination. — ^A well developed, well nourished, cheerful, and healthy
looking young woman. Pasty complexion with some acne. On closer examina-
tion flabbiness of superficial tissues indicates loss of weight. Teeth normal.
Tonsils barely visible. Thyroid a trifle prominent. Epitrochlear and axillary
glands are the only ones palpable. Reflexes active. General examination
negative.

378 CHAPTER III

Treatment. — Sugar and ferric chloride reactions continued very heavy with the
observation diet of 100 gm. protein, 5 gm. carbohydrate, and 2000 calories on Oct..
16. They proved stubborn, and 9 days of fasting were necessary, glycosuria
being absent during the last 36 hours. 300 cc. soup and 300 cc. coffee were
allowed daily during fasting, but no alkaU or alcohol was given. Fasting was
borne without disturbance, and the patient went shopping and to matinees and
remained strong and cheerful throughout. Green vegetables were begun in the
usual manner on Oct. 26, with addition of 10 gm. carbohydrate daily, until glyco-
suria appeared with 90 gm. carbohydrate on Nov. 5. The protein-fat tolerance
was low, for traces of both sugar and diacetic acid recurred with undue frequency
on the subsequent carbohydrate-free diet of 66 gm. protein and 1250 calories.
Colds, due to the winter weather, were responsible for part of the trouble. In
particular an acute coryza was the occasion for the well marked sugar and ferric
chloride reactions of Dec. 14 and IS. Treatment was not complete, but the cli-
mate evidently disagreed, and as the home conditions were good, the patient
was discharged to return south on Dec. 17.

Acidosis. — No acute symptoms were present, but chronic acidosis was indicated
by the intense ferric chloride reaction, the ammonia nitrogen of 0.8 to 1.4 gm.,
and the plasma bicarbonate of 44.7 per cent. All these signs improved with fast-
ing, and by Oct. 28, early in the carbohydrate test, the ferric chloride reaction
was negative and the ammonia and CO2 normal. Thereafter on carbohydrate-free
diet the CO2 tended to remain on the lower, and the ammonia on the upper
normal limits. The ferric chloride reaction showed the peculiarities characteristic
for a diet barely at the edge of tolerance. Traces recurred from time to time,
sometimes with glycosuria, sometimes alone. In no instance was there any
loss of sugar from the body sufficient to account for these reactions, which appar-
ently corresponded to slight fluctuations in the diabetic condition.

Blood Sugar. — On Oct. 16, the sugar in whole blood was 0.416 per cent, in plasma
0.434 per cent. Oct. 21, after 4 days of fasting, it was down to 0.384 per cent in
the whole blood. The figure of 0.5 per cent in the plasma on that day is a dis-
crepancy which would indicate a very low sugar content in the corpuscles. A
similar, but less extreme discrepancy was .also seen on Oct. 23. In the next
few days marked fluctuations occurred, between 0.238 and 0.4 per cent, though
aU blood samples were taken in the morning fasting. On Nov. 1, the combination
of 0.145 per cent in whole blood and 0.312 per cent in plasma is proof of a mis-
take, and the possibility must therefore be admitted that these analyses were not
adequately checked. The poor protein-fat tolerance was indicated by the sharp
rise in h3rperglycemia, the highest figures of the series being reached with 0.426
per cent in whole blood and 0.464 per cent in plasma on Nov. 11. On the morn-
ing of Nov. 15, after a fast-day, the percentage was down to 0.185 ia whole blood
and 0.158 in plasma. Normal values were never attained, and the tendency was
toward marked hyperglycemia, the analyses on Dec. 16, before discharge, still
showing 0.185 per cent in whole blood and 0.222 per cent in plasma. The high
blood sugars and recurrent traces of glycosuria indicated that the condition had
not been brought adequately under control.

CASE RECORDS 379

Weight and Nutrition.— The weight at admission was 48.4 kg., at discharge
42.3 kg., the treatment representing undernutrition to the extent of 5.2 kg.
The patient was thus below average normal flesh, but the nutrition was still
adequate and the strength and spirits, which were good at admission, were per-
ceptibly improved. The diet prescribed at discharge contained 85 gm. protein
and 1250 calories, with thrice cooked vegetables for bulk (nearly 2 gm. protein
and 30 calories per kg., diminished by weekly fast-days to about 0.7 gm. protein
and 26 calories average).

Subsequent History. — As usual with incomplete treatment, the condition be-
came worse instead of better, and the patient was readmitted Jan. 5, 1916, after
having shown glycosuria most of the time at home.

Second Admission. — ^Weight was almost the same as at discharge. Heavy gly-
osuria was present, but the ferric chloride reaction remained negative, and a
slightly high ammonia was the only evidence of acidosis. Instead of an immedi-
ate fast, 3 days of carbohydrate-free diet of 620 calories were given; then a single
fast-day stopped the glycosuria. Green vegetables being then begun, a trace of
glycosuria appeared after 70 gm. carbohydrate. Protein-fat diet was then started,
and freedom from glycosuria was maintained thereafter only by continued ex-
clusion of carbohydrate and Kmitation of the diet to about 60 gm. protein and
1100 calories. The glycosuria on Apr. 11 to 12 and 15 to 16 was due to slight
violations of diet. The patient was discharged Apr. 29, 1916, upon her own in-
sistence on account of homesickness.

Acidosis. — In the general absence of indications on the part of the CO2 capacity
and the ferric chloride reaction, the only evidence was a sUghtly high ammonia.
With the carbohydrate period in Jan. this fell to a fuUy normal level. Also on
Feb. 7, followiftg a fast-day, the output was rather low. The last recorded
analyses showed 0.8 to 1.12 gm. daily.

Blood Sugar. — Hyperglycemia was continuous. The renal threshold was evi-
dently high. Even without glycosuria, the blood sugar curve was such as to
demonstrate inadequate control of the condition.

Weight and Nutrition. — The weight at this admission was 43.4 kg., at discharge
41 kg.; i. e., a loss of 2.4 kg. in nearly 5 months in hospital. The strength and
spirits were perceptibly impaired. The decline was no greater than might be
expected from gradual deterioration during such a time in a case of only partially
controlled diabetes. Probably better results as to strength, and certainly a very
different influence upon the diabetic condition, would have resulted from sharp
undernutrition to the degree necessary to bring the condition under control at the
outset, followed by a diet of perhaps the same caloric value actually given, but
which might then have been better tolerated. As usual, the attempt to keep
up the highest possible nutrition brought only the necessity of diminishing nu-
trition continually further. The diet prescribed at discharge was carbohydrate-
free, with 70 gm. protein and 1000 calories (1.7 gm. protein and 24.4 calories
per kg., diminished to about 1.5 gm. protein and 21 calories average by the
weekly fast-days, some of which were not quite absolute).

380 CHAPTER in

Sttbsequent History. — ^The patient remained nearly sugar-free for several months,
but traces of glycosuria recurred rather frequently from trivial or unknown causes.
In June, edema came on to a troublesome degree. After June 18, it became
impossible to control the glycosuria except with fast-days, though it remained
very small in amount. The patient was advised to return to the hospital, but
seemed better in Sept., and therefore did not return until Oct. 14. At home
her time was spent reading, sewing, driving, and preparing her meals. She was
thin, but there was no discomfort, except worry and mental depression over her
condition.

Third Admission. — The weight was 43.6 kg., but the apparent gain was due to
edema, and there had obviously been some loss of flesh. The general condition
was poorer than before. On a diet of 70 gm. protein and 600 to 800 calories, there
was excretion of IS to 19 gm. sugar and 4 or 5 gm. total ketones (as acetone), with
26.7 mg. total acetone per 100 cc. in the blood plasma, and CO2 capacity 63.1
per cent. Instead of fasting, the diet for 4 days was limited to green vegetables,
beginning with 25 gm. carbohydrate and diminishing to 2.8 gm., with the result
that glycosuria stopped, and total acetone was diminished to 1.35 gm. in the
urine and 15.7 mg. per 100 cc. in the plasma. The CO2 capacity remained high.
Protein-fat diet was then begun very gradually, at first with only 30 gm. protein
and 300 calories. After about 2 weeks of such undernutrition, the total acetone
remained consistently at 0.35 to 1.2 gm. in the urine and 8.3 to 17.3 mg. per 100
cc. in the plasma. Though glycosuria was absent the blood sugar on Oct. 16 to 21
was 0.244 to 0.20 per cent, plasma sugar 0.29 to 0.27 per cent. The weight by
the 1st of Nov. was down to 35 kg., largely through loss of edema, salt-free diet
being employed part of the time. Beginning early in Nov. the total calories
were increased gradually as high as 700 to 800, of which usually 175 were in the
form of brandy. The patient was discharged on Nov. 11, 1916, still weighing 35
kg. For continuance of undernutrition the diet prescribed was 35 gm. protein
and 875 calories, of which 175 calories were alcohol (1 gm. protein and 25 calories
per kg., reduced by the weekly fast-days to about 0.86 gm. protein and 21.5
calories average).

Subsequent History.— The patient remained sugar-free imtil about Christmas,
then glycosuria began to recur frequently. She was also weaker and more de-
pressed. She was readmitted to hospital Jan. 20, 1917.*

Fourth Admission. — The weight was 36.6 kg., partly edema. Glycosuria and
ketonuria were present, but as the condition was so far advanced, the staff mem-
ber in charge chose not to dear it up. The diet was raised to 50 to 55 gm. protein
and 1100 to 1380 calories, with slight subjective improvement. The stay in
hospital continued until Feb. 21, 1917. No immediately threatening symptoms
appeared, and the patient was about and outdoors part of each day as before.
At discharge the weight remained approximately 35 kg.; weakness and discomfort
were progressive.

Subsequent History. — ^The patient continued to be more. uncomfortable than
when sugar-free. It was impossible for her to take the more liberal diet which

CASE RECORDS 381

had been granted, because eating practically anything made her nauseated.
Under a local physician her diet on this account was less in quantity than before,
but active diabetes continued. Death occurred Apr. 26, 1917, in coma.

Remarks. — The history is a typical one for many diabetic patients. There
was first the long period of mild glycosuria, when the favorable opportunity
for effectual treatment was allowed to slip by. The onset of a more severe
stage seems to have been rather sudden. The physician in charge then em-
ployed radical measures, but these were not wholly adequate at this stage. As
so frequently occurs, the patient was sent for a specialist's care when the condition
was already too far advanced for any genuinely good result to be possible from
dietetic measures. The severity was such that only the most rigorous program
could have brought it under control, and there was the usual hesitation about
taking a patient seemingly in fair condition and reducing weight and strength
to the requisite degree. When more radical undernutrition was attempted in
the third period in hospital, it was too late, and it is possible that the assimila-
tive function was absolutely too low to support life. If the patient even at the
first admission to hospital had been promptly reduced to the weight and diet to
which the downward progress later brought her, the opinion may be ventured
that she not only would have lived longer, but also this same period between
Oct., 1915, and Apr., 1916, would have been characterized by a higher average of
strength, comfort, and usefulness.

CASE NO. S3.

Female, age 9 yrs. American; schoolgirl. Admitted Oct. 15, 1915.

Family History. — Parents well, except that mother is nervous. One sister well.
No diabetes or heritable disease known in family.

Past History. — Healthy life in good hygienic surroundings in a small town in
the middle west. Measles, mumps, chicken-pox in early years. No tonsillitis for
2 years past; 4 or 5 attacks before that. Stiffness and pain in various joints at
times, but no definite rheumatism. Child has made average record at school.
Nervous disposition. Development normal; not obese.

Present Illness. — Polyphagia, polydipsia, and polyuria began 2 years ago. Un-
der a specialist's care in a Chicago hospital, glycosuria was cleared up on restricted
diet without fasting. Sugar-freedom was maintained until last Feb.; since then
glycosuria has been continuous. Pruritus vulvae for past 4 months.

Physical Examination. — Height 125.2 cm. A fairly developed but emaciated
child, pale and weak. Mouth and throat negative. No notable lymph gland
enlargement. Reflexes normal. General examination negative.

Treatment. — A 5 day fast was necessary to clear up glycosuria. On the usual
green vegetable period, glycosuria appeared on Oct. 30 with 80 gm. carbohydrate.
Thereafter a diet of 1000 calories with small quantities of carbohydrate was badly
assimilated from the standpoint of hyperglycemia and occasional traces of glyco-
suria. Carbohydrate was omitted beginning Dec. 10, the usual diet being 40

382 CHAPTER in

gm. protein and 600 to 800 calories, with routine weekly fast-days. A second
carbohydrate test beginning Jan. 24 showed increased tolerance; glycosuria ap-
peared with 120 gm. carbohydrate on Feb. 5. By Feb. 21, the patient was able
to assimilate a diet of 40 gm. protein, IS to 20 gm. carbohydrate, and 750 calories.
She was discharged Feb. 24 on this diet, except that only 10 gm. carbohydrate
were permitted.

Acidosis. — No threatening symptoms were present at any time, but the heavy
ferric chloride reaction and the CO2 capacity of 37 per cent at admission were
significant. Both these signs changed rapidly for the better on fasting, and on
carbohydrate and mixed diet thereafter. With normal CO2 and negative ferric
chloride, the ammonia excretion still showed a slight acidosis in Dec. and Jan.
This gradually diminished to a normal level by the time of discharge.

Blood Sugar. — There was evidently a far greater excess of plasma sugar over
corpuscle sugar on Oct. 26 than at later periods. The salient feature is the steady
decline of the blood sugar curve toward normal. The reason for the occurrence
of h)rperglycemia in the last analysis on Feb. 24 is not known.

Weight and Nutrition. — The weight was 20 kg. on admission, 16.9 kg. at dis-
charge; i. e., a loss of 3.1 kg. The child was emaciated at admission, and never
showed improvement of appearance in consequence of treatment. Exercise was
employed dvuing most of the period in hospital. It afiEorded the child a more
normal and enjoyable life, but did not build up tolerance appreciably or confer
real strength. It may have been one factor along with the low diet in bringing
down the blood sugar. There was one cold while in hospital; glycosuria did not
result, and recovery imder the low diet was normal. The diet prescribed at dis-
charge represented about 2.4 gm. protein and 44 calories per kg., diminished to
about 2.1 gm. protein and 38 calories average by the weekly fast-days. The diet
therefore was absolutely low, but adequate as reckoned on the greatly reduced
weight. The child was regularly up and about all day long, and amused herself
with active play and other occupations, but always kept the appearance of a
little invalid.

Subsequent History. — The patient remained free from glycosuria, except for rare
traces due to accidents of diet and one attack of grippe. By Sept. 9, she had im-
proved sufficiently to begin school, but weighed only 17.7 kg. Toward the end
of Sept. she had a severe cold, and another in Oct. with temperature of 101.5°.
Both caused glycosuria, and thereafter permanent sugar-freedom was difficult
to maintain. She was advised to return to the hospital, but the parents delayed,
and death occurred in coma on Jan. 25, 1917.

Remarks. — ^This was one of the worst cases among the children in this series,
not only because of the low food tolerance, but also because of the frailness of the
patient, whose whole appearance indicated exhaustion and low resistance. The
diets were never excessively low, even those in the forepart of Jan. representing
about 2.2 gm. protein and 36 calories per kg. for 18 kg. weight. The general
result of treatment, by reason of the fasting and carbohydrate periods and
exercise, was the above mentioned loss of 3.1 kg. during more than 4 months

CASE RECORDS 383

in hospital. Durmg 7 months thereafter at home, the weight showed a slight
increase.

It is noteworthy that in a case of this very unpromising type a demonstrable
increase of carbohydrate tolerance was produced in hospital, and also all symptoms,
including hyperglycemia, were brought under control. No upward progress or
actual recovery of assimilation was demonstrated; the improved tolerance was
merely purchased at the price of diminished weight. But even with the neces-
sarily unfavorable conditions, downward progress came only with an infection
approximately 1 year from the time the patient was first received. The record is
satisfactory to the extent that both life and comfort were evidently prolonged by
treatment in an unpromising type of case.

CASE NO. 54.

Female, married, age 29 yrs. American; telephone operator. Admitted Oct.
16, 1915.

Family History. — Mother died with a "severe cold" in 1891. Father is well.
One brother died of meningitis in childhood; eight brothers and sisters are well.
Husband well. No diabetes or other heritable disease in family.

Past History. — Measles and whooping-cough in childhood. No other illnesses;
no sore throats. Healthy life. No nervousness. Appetite, diet, and digestion
normal. Menstruation normal. One miscarriage 3 years ago; no other pregnancy.

Present Illness. — June 1, 4| months before admission, patient weighed 144
pounds and felt so well and free from strain that she went on with work instead
of taking summer vacation at the usual time. Within 2 weeks from that time
and with no illness or other disturbance of any kind, polydipsia and polyuria
began, and there has since been progressive loss of strength and 30 pounds weight.
Patient was first seen by a doctor and diabetes diagnosed on July 4. Under
gradual withdrawal of carbohydrate she became free from glycosuria on Aug. 13
and remained so until Sept. 12, since when glycosuria has been present except on
fast-days.

Physical Examination. — Height 169 cm. A well developed and fairly nourished
woman, with no striking symptom except dyspnea and acetone odor. Mouth and
throat normal. Abdomen slightly distended and tympanitic. Kjiee jerks sluggish .
Blood pressure 110-80. General examination negative. Wassermann negative.

Treatment. — Impending coma was indicated by the dyspnea, heavy ferric chlo-
ride reaction, ammonia nitrogen of 2.52 gm., and CO2 capacity of 29 per cent. A
light observation diet was given, with SO gm. sodium bicarbonate in the evening.
The next day fasting was begun, with 300 cc. each of coffee and clear soup and 286
calories of alcohol daily. 30 gm. sodium bicarbonate were given on Oct. 17 and
19, 20 gm. on Oct. 20, and 15 gm. on Oct. 21. Glycosuria was absent after the
21st. On Oct. 22, 10 gm. carbohydrate were given in the form of lettuce, celery,
and tomatoes; 20 gm. on the 2 succeeding days, and 14 gm. on Oct. 25. Glyco-
suria was continuous on this low intake, but was checked by the fast-day of

384 CHAPTER m

Oct. 26. On Oct. 27, 10 gm. carbohydrate were given, and increased by 10 gm.
daily, glycosuria appearing with 40 gm. carbohydrate on Oct. 30, and continuing
with diets of SO to 30 gm. protein, 10 gm. carbohydrate, and 1000 to 800 calories
on the following day. At first the patient had given the impression of a mod-
erately severe diabetes with threatened coma, but now the case looked more
serious when it appeared that the food tolerance was ahnost zero. Ketonuria,
though diminished, persisted. Hyperglycemia was stubborn, and between Nov.
10 and 20 it was found that carbohydrate-free diets of 40 gm. protein and 800
calories sufficed to keep up almost continuous glycosuria. Nov. 21 was a fast-
day with only 70 calories alcohol. On the following 3 days, 10 to 20 gm. car-
bohydrate in green vegetables were the only food. On Nov. 25 and 26, 40 gm.
protein, S gm. carbohydrate, and 800 calories were given. Still glycosuria and
ferric chloride reactions persisted. The former was stopped and the latter
diminished by 3 fast-days, Nov. 28 to 30. Then, beginning with 5 gm. carbo-
hydrate on Dec. 1 , green vegetables were increased daily, until glycosuria appeared
with 40 gm. carbohydrate on Dec. 5. On Dec. 8 to 11, carbohydrate-free diets of
60 to 25 gm. protein and 800 to 325 calories kept up marked glycosuria and keto-
nuria which did not cease even with 3 fast-days (Dec. 12 to 14). On Dec. 15
and 16, 30 to SO gm. protein and 170 to 305 calories were given, with continued
glycosuria and ketonuria. Dec. 17 and 18 were fast-days with cofifee, soup, and
315 calories alcohol, and both sugar and ferric chloride reactions became nega-
tive. With continuance of the same liquids, one egg was allowed on Dec. 19 and
two eggs the next day, and glycosuria and ketonuria remained absent on an increase
up to five eggs on Dec. 25 (714 calories, 315 of which were alcohol). A pre-
cautionary fast-day with whisky was given on Dec. 26, then the diet again in-
creased until continuous glycosuria appeared on 45 gm. protein and 1025 calories
(315 alcohol, 710 food) following Dec. 30. The fast-day on Jan. 2 checked the
glycosuria, but it reappeared on a diet of 45 gm. protein and 888 calories (alco-
hol 315, food 573). The menu for such a day, characteristic of the diets on which
it was necessary to keep this patient, was as follows:

60 gm. bran. 6 eggs.

300 cc. coffee. 10 gm. olive oil.

300 " soup. 100 " thrice cooked asparagus.

90 " whisky. 100 " " " spinach.

Again reUef from glycosuria was given by a fast-day on Jan. 9, and on the 11th
glycosuria reappeared on four eggs, 300 cc. coffee, 450 cc. soup, and 90 cc. whisky
(30 gm. protein and 634 calories) — no vegetables, bran, or any source of carbohy-
drate. On the following days, it became certain that the patient definitely could
not tolerate the protein of four eggs. The fast-day of Jan. 16 failed to stop the
glycosuria, therefore (Jan. 21 to 25) 5 successive days of fastmg and alcohol were
imposed. On Jan. 26 one egg was added, on Jan. 28 two eggs, on Feb. 3 three
eggs, m addition to 200 gm. thrice boiled vegetables and 525 calories of alcohol.
The chart shows the continuous slight glycosuria, not stopped by the fast-day of

CASE RECOEDS 385

Feb. 6. Reduction to one egg on Feb. 10 and fasting the next day stopped the
glycosuria, but it returned when the eggs were increased to three on Feb. 15.
The remainder of the long graphic record shows practically the same story of con-
tinuous inabihty to tolerate anythmg approaching a livmg diet. On some occa-
sions, the Umit of tolerance was only two eggs without other food, three eggs causing
glycosuria. On this account alcohol was pushed to a maximum of about 500
calories, to keep up nutrition as well as possible. Beginning with a fast-day
on June 13, another carbohydrate period was tried. By June 18, 25 gm. carbo-
hydrate were taken without glycosuria, but the patient's strength had collapsed
and a change to other food was imperative. Accordingly on Jvme 19, the 8 month
attempt to control the condition was abandoned. Glycosuria was present on the
carbohydrate-free diet of 36 gm. protein and 1000 calories (490 alcohol, 590 food).
It increased, and ferric chloride reactions promptly returned, when the diet was
raised to 45 gm. protem and 1490 calories (490 alcohol, 1000 foo'd). An alarming
fall in the blood bicarbonate promptly followed, down to 28.7 per cent on June
29. To meet the combination of extreme weakness and impending coma, alcohol
and protein were continued the same and the fat diminished to make a total
ration of only 900 calories. The threatening symptoms passed off, and without
the use of alkali the CO2 capacity had risen to 61 per cent by July 6. The fat
was increased to make the same 1490 calories as before. Meanwhile also car-
bohydrate had been introduced up to 17.5 gm. daily. With the increase in fat
came another sharp fall of the CO2 capacity, so that on July 12 it was 35.9 per cent.
40 gm. carbohydrate were given on that day without clinical benefit. Resort
was had to fasting to avert the imminent coma. On July 13, the only food was 7
gm. carbohydrate and 70 cc. whisky; on the 14th only whisky was given; on the
15th, 15 gm. protein were added. By this time the CO2 capacity was up to 62.5
per cent, again without the aid of alkali. July 16 was a fast-day, and on the
17th the diet was 30 gm. protein, 20 gm. fat, and 35 cc. whisky; 430 calories in
all. On the 18th, the patient awoke clearly conscious, but weak. She went into
collapse with loss of consciousness, and died from final exhaustion of strength at
2:40 p.m. Death occurred with insignificant ammonia, negative sugar and
ferric chloride reactions, and normal plasma bicarbonate as far as can be judged
by the last analysis on July IS. There were no symptoms suggesting diabetic
coma, and the unconsciousness was merely such as precedes death from starvation.
Acidosis.— This patient always responded to fasting with a quick clearing up of
acidosis. The ferric chloride reaction was stubborn for about 2 months, then
remained almost continuously negative until the final period of overfeeding in
June. The plasma bicarbonate maintained a normal level throughout most of the
time. A more dehcate index of the slight acidosis was frequently found in the
sUght elevation of the ammonia output. Aside from the bicarbonate dosage on the
first few days as mentioned, no alkaU was used. A sharp fall in the CO2 capacity
in Jan. (62 per cent on )the 15th, 56 per cent on the 17th, 44.2 per cent on the
19th, 43.2 per cent on the 25th) occurred without known cause or disturbance.
By Feb. 2, it had risen spontaneously to 56.6 per cent. The terminal record in

386

CHAPTER ni

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Fat 58.7
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Alcohol 70.0
Calories 1231

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Fat 33.1
Carbohy-
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Alcohol 70.0
Calories 1026

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388

CHAPTER III

June and July is of interest as showing how a low fat allowance brought on prompt
severe acidosis, not prevented by alcohol, nor on the second occasion by carbohy-
drate, but yielding very easily to simple withdrawal of fat both times (Table
XIV). The fat allowance bringing on the dangerous acidosis in each instance
was rather high in proportion to the weight of the extremely emaciated patient,
but in absolute quantity was very low. It is evident that the production of acido-
sis cannot be attributed to protein, because it developed on 35 to 60 gm. protein
in the period June 14 to 28 and cleared up on 50 to 55 gm. protein in the period
June 29 to July 6. Diets predominantly protein, as those of July 13 to 17, acted
favorably in diminishing acidosis, but protein was not indispensable for the pur-
pose, as fast-days always acted favorably in this patient. Carbohydrate was
scarcely important in checking the acidosis, since the quantities in the period
June 29 to July 6 were so small, and acidosis similarly was controlled on July 15
without carbohydrate. The influence of alcohol was not perceptible; acidosis
was controlled as readily on 35 gm. alcohol as on 70 gm. It is clearly evident
that the giving or withholding of fat was the sole determining factor in producing
and abolishing acidosis, and the specially noteworthy point is the small absolute
quantity of fat which was effective for this purpose.

Blood Sugar. — The marked and stubborn h)rperglycemia, and the response of
both blood sugar and glycosuria to sHght changes in the diet, proved that actual
severity of diabetes was the sole cause of difficulty, and not altered renal per-
meability. Normal blood sugar was attained on only a few occasions. On Dec.
2, there was a practically normal reading for the whole blood, but hyperglycemia
in the plasma, as if the corpuscles were almost sugar-free. Both were normal on
Apr. 5. The low normal figure before breakfast on June 18 doubtless represented
extreme exhaustion rather than genuine improvement in the diabetes.

Weight and Nutrition. — This was the most extreme imdemutrition in the entire
series. The patient appeared well nourished at a weight of 49 kg. at admission,
and died of inanition 9 months later at a weight of 24 kg.; i. e., a loss of 25 kg.
since admission, and 41 kg. since the onset of diabetes.

The nitrogen analyses show a fairly uniform excretion of about 8 gm. daily.
The negative balance during this time was not so great as will appear from the
comparison of intake and output, because the nitrogen of the soup was not in-
cluded in the dietary record. As no fecal analyses were done, an exact reckoning
of the balance is impossible. Concerning the total energy intake, the following
calculation can be made.

276 days.

Per day
(average).

Per day
per kg.

Alcohol calories

90,348
96,692
187,040
7,305 gm.
6.881 "

315.6
362.1

677.7
26.4 gm.
24.8 «

9 6

Food "

10 9

Total "

20 5

Protein in diet

0.80 gm.
0 75 "

Fat " "

CASE RECORDS 389

On Mar. 31, this patient was studied in the respiration calorimeter by DuBois
and collaborators, who determined the following.' "I. Her total metabolism is
the lowest recorded in the literature, being only 23.3 calories per square meter
per hour, which is 37 per cent below the average basal normal in women. Since
her original weight with clothes had been 66 kg., one may be permitted to assume
a weight of 62 kg. without clothes. Had her metaboUsm been normal for this
weight, it would have been 63.3 calories per hour instead of 29.4 calories, which
were actually measured when her weight had fallen to 32. S kg. The extreme
emaciation which had resulted m a reduction of body weight to nearly haU of
what it was originally, reduced the metabolism so low that only 40 per cent of
the origmal heat production was necessary for life. II. The nitrogen excretion
in the urine (0.39 gm. per hour) is the quantity commonly found in normal
people. The total metabolism, however, is so low that the percentage of calories
from protein is quite high, 35 per cent (IS per cent being the average normal).
III. The respiratory quotients average 0.82, a normal figure. From this, one
may calculate that fat gives 39 per cent of the calories of metabolism and car-
bohydrate 26 per cent. This corresponds to the utilization of 44 gm'. of carbo-
hydrate daily, and smce none was given in the food, these results are difficult to
interpret."

The patient's total heat production at this time was 29.5 calories per hour, or
708 per day. Presumably it was somewhat higher in the preceding months, and
probably by June 15 had fallen even lower. If this 708 calories be taken as an
average for comparison with the average intake of 677.7 calories above calcu-
lated, it is seen that the diet is deficient notwithstanding the great lowering of
metabohsm, and even without allowance for any loss through the feces. The
nitrogen excretion of 0.39 gm. per hour in the calorimeter experiment represents
an actual catabohsm of 58.5 gm. protein per day, with no allowance for any specific
dynamic action of ingested protein. There is a serious discrepancy between this
and the average protein intake of 26.4 gm. There was thus a continuous consump-
tion of both body fat and body protein in the process of slow starvation.

Lipemia. — ^Heavy and continuous Hpemia was present at admission, gradually
clearing up during the fasting and carbohydrate period. Thereafter the plasma
remained clear until the terminal period in June and July, when hpemia reap-
peared and persisted in its original intensity. A noteworthy feature is the very
limited fat intake which sufficed to produce such a heavy hpemia under these
circumstances. No analyses were made.

Dextrose Nitrogen Ratio. — -This was the type of case which could almost certainly
be counted upon to show "total" D:N ratios, if the active symptoms had been
allowed to gain fvdl headway. The condition was held under control sufficiently
that this ratio was never observed, the ratios in the terminal period of glycosuria

' Gephart, F. C, Aub, J. C, DuBois, E. F., and Lusk, G., Metabolism in Three
Unusual Cases of Diabetes, Arck. Int. Med., 1917, xix, 908-930.

390

CHAPTER m

being never higher than 2.36, as shown in Table XV. This calculation is also
confused by the unknown quantity and character of the nitrogen in the soup.

Remarks. — This case at the time was regarded as a unique example of
spontaneous downward progress, residting from some special factor. Strong
suspicions were entertained that this might be an infectious or mahgnant process,
probably tuberculosis, but repeated examinations by members of the staff and
outside consultants failed to reveal any evidence of such lesions. Necropsy was
positively refused, so this important point could not be settled. Experience with
similar or worse cases since the dose of this series indicates that they merely
represent diabetes of extreme severity, very susceptible to downward progress
when the trivial tolerance is overtaxed by diets such as described or even lower.

TABLE XV.

Date.

Urinary' sugar.

Total nitrogen.

D:N ratio.

ifie

gm.

gm.

June 27

21.60

9.15

2.36

" 28

23.95

11.02

2.17

" 29

15.84

8.10

1.96

" 30

18.85

12.43

1.52

July 1

24.67

—

—

" 2

29.15

—

—

" 3

25.80

9.47

1.33

" 4

32.86

11.30

1.74

« 5

—

11.55

—

" 6

23.00

11.21

0.87

" 7

20.50

—

—

" 8

34.48

11.27

1.37

" 9

37.70

9.84

1.89

" 10

18.70

• ^~'

—

They are controllable only by such remarkably severe undernutrition as wiU
maintain continuously normal blood sugar, and even with the most rigid treat-
ment the metabolic function may be found actually too low to support life.

CASE NO. 55.

Male, age 26 mos. American. Admitted Nov. 3, 1915.

Family History. — Father aged 32, mother 26; both healthy. Patient is the
only child. A paternal great grandmother died of diabetes. No other heritable
disease known in family.

Past History. ~k normally delivered, healthy child with no mfectious history
whatever.

CASE RECORDS 391

Present Illness. — After gradual increase of polyphagia, polydipsia, and polyuria
for 3 weeks, the father, a physician, made a urine analysis Oct. 26 and found
heavy glycosuria. Treatment has consisted in a diet of 2 to 5 pints of milk and
one poached egg daily. For a few days before admission the child has been acting
cross and unwell. No. sleepiness or dyspnea until the past day or two.

Physical Examination. — A well developed, well nourished child. Decided
drowsiness, but no dyspnea. Hectic flush of cheeks. Tonsils moderately hyper-
trophied. Reflexes normal. Epitrochlear glands palpable. Otherwise fully
normal to examination. Wassermann reaction of patient and both parents
negative.

Treatment. — The patient was admitted just before noon Nov. 3, and received
that day an observation diet of 1400 cc. milk. As the urinary findings and low
CO2 capacity showed danger of coma, the diet on the following 2 days was only
13.S gm. protein, 20 gm. carbohydrate, and 280 calories, mostly as milk, with 600
to 800 cc. clear soup additional for the sake of fluid and salts. Fasting was then
imposed, Nov. 6 to 9. Green vegetables were then begun and increased in the
usual manner, and on Nov. 13, 40 gm. carbohydrate were thus taken without gly-
cosuria. This diet was stopped to avoid too long undernutrition of such a young
child, and also because edema was causing worry to the mother. After a fast-
day on Nov. 14, a mixed diet of 25 gm. protein, 20 gm. carbohydrate, and 675
calories (including 400 cc. milk) brought on glycosuria. After a fast-day on Nov.
21, a diet of 44 gm. protein, 10 gm. carbohydrate, and 550 calories was assimi-
lated without glycosuria. But on Nov. 29 to 30 an increase to 47 gm. protein,
15 gm. carbohydrate, and 612 calories brought glycosuria on the 30th. The pa-
tient was discharged on Dec. 9 ia apparently perfect health, with all chemical
findings normal.

Acidosis. — ^Acidosis threatening coma cleared up promptly on fasting. As chil-
dren are supposed to show fasting acidosis very readily, notice may be taken of
the fact that on the last day of the 4 day fast (Nov. 9) the ferric chloride reac-
tion was fuUy negative, and the plasma bicarbonate had risen to 50.4 per cent,
approximately normal for a young child. Signs of acidosis remained entirely
absent thereafter. No alkali was used. An experience near the beginning gave
an interesting illustration of the effect of food. The low diet shown in the chart
for Nov. 4 was only breakfast. Fasting was then begim because of threatening
coma sjonptoms. By the next morning the clinical improvement was very evi-
dent, and the CO2 capacity showed a rise from 30.4 to 40.3 per cent. Dxuring
this day of Nov. 5 the child received by mistake a tray intended for a cardiac
patient, reprefeeinting 18 gm. carbohydrate and 15 gm. each of protein and fat.
The record shows how not only was glycosuria increased, but the CO2 capacity
by the next day was depressed to 32.6 per cent, notwithstanding the large pro-
portion of carbohydrate and protein in the food. Resumption of fasting promptly
cleared up acidosis as described.

Blood Sugar. — The very high value of 0.57 per cent at admission was due to
the high carbohydrate diet. The immediate fall on fasting was characteristic

392 CHAPTER m

both of h}fperglycemia due to carbohydrate and of early diabetes. The analyses
of Nov. 10 would indicate that the corpuscles retained sugar longer than the
plasma. A prompt fall to normal was easily obtained, and the subsequent figures
for blood sugar in the morning before breakfast were fuUy normal. Analyses
during digestion would doubtless have shown h3fperglycemia.

Weight and Nutrition. — In a little over 1 month in hospital the weight was
reduced by 1 kg. The rise of weight shown in the fasting and carbohydrate
period was due to well marked edema. The diet prescribed at discharge was 45
gm. protein, IS gm. carbohydrate (10 in milk, 5 in vegetables), and 575 calories
(about 4.1 gm. protein and 52 calories per kg., reduced by fortnightly fast-days
to 3.8 gm. protein and 48 calories per kg.). As compared with standard diets
for children, this one was deficient in carbohydrate, but sufficiently abundant in
other respects to assure gradual aggravation of the diabetes.

Subseqzient History. — The patient remained free from glycosuria, regained nor-
mal behavior and activity, and for exercise coasted with his sled, walked, and
climbed as many as 20 flights of stairs daily. On Jan. 12, the sugar in whole
blood was 0.119 per cent, in plasma 0.159 per cent. There had been a gain of
0.3 kg. weight and 0.3 cm. height. Later in Jan. an attack of grippe brought on
glycosuria, which was cleared up by fasting 3 days. Thereafter it was absent
on a diet containing only 5 gm. carbohydrate. On Feb. 5, heavy glycosuria ap-
peared without apparent cause. Thereafter 1 fast-day was given every week.
Mar. 9, glycosuria again returned, and thereafter was more persistent. The
patient was readmitted on Apr. 15 because of the difficulty in maintaining sugar-
freedom.

Second Admission.-^The weight was 0.1 kg. greater than at discharge, the
height 87.7 cm., a gain of 1.7 cm. since the first measurement (Nov. 15, 1915).
The appearance and behavior were excellent, and there were no subjective symp-
toms. Notwithstanding the trace of glycosuria, the fasting blood sugar had
fallen to normal (0.095 per cent in whole blood, 0.110 per cent in plasma, CO2
capacity 52.5 per cent; on the next morning 0.069 per cent in whole blood, 0.070
per cent in plasma, CO2 capacity 49.8 per cent). Green vegetables were begun
after a day of fasting, adding 10 gm. carbohydrate daily, and glycosuria appeared
on 90 gm. carbohydrate. The blood sugar, mornings before breakfast, continued
normal, hyperglycemia evidently being brief following carbohydrate ingestion.
The CO2 capacity rose markedly to 60.6 per cent, perhaps partly because of the
carbohydrate and partly because of the alkaline diet. After a fast-day on Apr.
27, a diet of 40 gm. protein, 15 gm. carbohydrate, and 575 calories was assimi-
lated without glycosuria. Glycosuria occurred on May 3 and 4, after the car-
bohydrate had been increased to 20 gm. beginning Apr. 30. In the last analyses
preceding discharge, the blood sugar contmued normal, the CO2 was slightly
low and the ammonia slightly high. The weight had been reduced to 10.5 kg.
The strength and spirits were excellent. The prescribed diet was the same as
at the previous discharge.

CASE RECORDS 393

Subsegiient History. — The patient showed glycosuria within the first few days
after leaving the hospital, and this recurred stubbornly from time to time not-
withstanding reduction to carbohydrate-free diet. The patient gradually de-
clined in weight and strength. Glycosuria was controlled by the parents by
means of fast-days and reduced diet. During June and July, on a trip to the
seashore, there was some gain in weight and strength. After Aug. the decline
was continuous. After Oct. the parents abandoned the attempt to maintain
sugar-freedom, but regiJated the diet carefully. From that time onward it
consisted of almost nothing but eggs. Feeding was carried on untU threatening
symptoms resulted; these were cleared up by fasting, and so on. Death occurred
Jan. 3, 1917.

Remarks. — Severe diabetes in a child of this age must often be hopeless under
any dietetic treatment. The result is satisfactory to the extent that the ordinary
duration of life in a patient of this type, according to the experience of Dr. Emmett
Holt, who referred the child here, was formerly not more than 3 months, whereas
in this patient excellent physical condition was maintained for at least 5 months
and the total duration of life from the time of admission was exactly 14 months.
The metaboUc strain of growth may be sufficient to account for downward pro-
gress; but a longer preservation of life and health with equal or better growth and
strength would probably be attainable on a lower diet containing a larger pro-
portion of carbohydrate.

CASE NO. 56.

Male, married, age 30 yrs. American; railway clerk. Admitted Nov. 3,
1915.

Family History. — Father died of an injury. Mother well at 73. One brother
is well. Of six sisters, two are well; one has severe, and another sUght rheumatoid
arthritis; the other two are weakly and anemic. One maternal aunt was tem-
porarily insane after worry, but recovered and enjoys good health at 75. No
diabetes or other heritable disease known in family.

Past History.— Healthy life with good hygiene. Whooping-cough in childhood.
Rather frequent gastrointestinal upsets with fever as a child. There were swollen
glands below the angle of the jaw on both sides in childhood up to the age of 12
or 14; they became inflamed whenever patient had a cold. Enuresis up to 12 or
14. No other illnesses. Married 6 years. Wife and only child healthy. Pa-
tient has been ahnost a total abstainer from alcohol. Has smoked moderately,
taken three cups of tea daily, and has been very fond of desserts and candy.
Chronic constipation.

Present Illness.— Grippe m the faU of 1912 was followed by weakness and de-
pression until Jan., 1913, when an examination showed glycosuria. Polyphagia,
polydipsia, and polyuria were then also present. On restricted diet he has re-
mained at work, but has continually lost weight and strength, until he is now
incapacitated.

394 CHAPTER ni

Physical Examination. — Height 183.8 cm. A tall, emaciated man without
acute symptoms. Teeth show caries, but no pyorrhea. Throat and tonsils nor-
mal. Cervical lymph nodes not palpable. Small, hard epitrochlear, axillary,
and inguinal nodes palpable. Blood pressure 100 systolic, 80 diastolic. Knee
jerks diminished. Examination otherwise negative.

Treatment. — Patient had been on restricted diet, with the consequence that he
showed only slight glycosuria but heavy ferric chloride reaction at admission.
2 fast-days on Nov. 6 and 7 suf&ced to abolish glycosuria. In the subsequent
test with green vegetables, glycosuria appeared with 90 gm. carbohydrate on Nov.
16. The carbohydrate period was prolonged to determine whether this was the
true tolerance, and also for the sake of prolonging undernutrition and diminish-
ing any latent tendency to acidosis. Mixed diet was then begun, and a
trace of glycosuria appeared on Dec. 11, after 3 days of 100 gm. protein, 60 gm.
carbohydrate, and 2000 calories. The patient was discharged on Dec. 20 with
urine normal.

Acidosis. — The ferric chloride reaction was abolished early in the carbohydrate
period. The plasma bicarbonate, which was down to 44 per cent on the morn-
ing of Nov. 8, after the 2 preceding fast -days, rose sharply within normal limits
by Nov. 11, and remained there except for a slight drop following the fast-day
of Nov. 23.

Blood Sugar. — There was the usual hyperglycemia at admission and fall on
fasting. The low values found on Nov. 24, after the fast-day of Nov. 23, fol-
lowing the undernutrition of the carbohydrate period, proved that the blood
sugar could be brought to normal. The subsequent treatment did not hold it
down. On the contrary, the last analysis on Dec. 8 showed 0.2 per cent plasma
sugar. This and the preceding analysis of 0.245 per cent (Nov. 10) without
glycosuria indicated a high renal threshold, especially as the percentages must
have been somewhat higher during the day than in the morning, and those in the
plasma were slightly higher.

Weight and Nutrition. — Weight at admission 51 kg., at discharge 48.2 kg.;
i.e., a reduction of 2.8 kg. The diet prescribed at discharge was 100 gm. pro-
tein, 50 gm. carbohydrate, and 1750 calories (about 2.1 gm. protein and 36 calories
per kg., reduced by the weekly fast-days to 1.7 gm. protein and 31 calories aver-
age). The patient felt greatly strengthened and benefited, and hoped to resmne
regular work after a vacation in the south. The imdernutrition, however, had
not been stringent enough to bring the. condition under control, as proved by
the marked hyperglycemia. Letting a half treated patient go on a diet as lib-
eral as this was a certain means of assuring a relapse. Considerable exercise was
required of the patient, both inside and outside hospital, but this had obviously
failed to bring the condition imder real control.

Subsequent History. — The patient caught cold shortly after returning home and
showed glycosuria, which he cleared up by fasting, but sugar returned when he
tried to resume even a lower diet than before. After having shown sugar most
of the time, he was readmitted Feb. 17, 1916.

CASE RECORDS 395

Second Admission. — Repeated fasting for clearing up glycosuria had brought
the weight down to 46.8 kg., a loss of 1.4 kg. since discharge. The plasma bicar-
bonate was approxunately normal, the ferric chloride reaction negative, while
the ammonia nitrogen of 0.87 gm. mdicated a slight acidosis. Fasting was be-
gun after breakfast on Feb. 19. Glycosuria promptly ceased, but reappeared
on diets of 80 to 100 gm. protem and 1500 calories, even though all carbohydrate
was excluded. Beginning Mar. 6, glycosuria was absent on 1200 calories with
.70 gm. protein and no carbohydrate; and subsequently 75 gm. protein, 15 gm.
carbohydrate, and 1700 calories were taken without glycosuria. The CO2 ca-
pacity stocid at low normal nearly all the time. Doubtless ammonia determina-
tions would have shown slight acidosis. The blood sugar was never brought to
a normal figure and was still 0.2 per cent when the patient was discharged on
May 3.

The patient felt well on the prescribed diet last mentioned. There had been
no undernutrition in consequence of either diet or exercise this time, since the
weight was the same as at admission. Accordingly, the condition had again
not been brought under any control, except for the transitory freedom from
glycosuria.

Subseqttent History. — Slight transitory glycosuria occurred with a cold in May.
It then remained absent, except for rare traces up to Aug. 18, when the patient
called to report. He was then planning to return to work. The next heard
from him was on Dec. 4. He had tired too easily on attempting to work, and also
glycosuria appeared. He tried to control his condition by modification of diet
himself, but finally reached the point of continuous glycosuria and downward
progress. He was readmitted to hospital Dec. 6, 1916.

Third Admission. — The weight was down to 43.4 kg.; i.e., a loss of 7.6 kg.
since the first admission and 3.6 kg. since the last discharge. Some edema was
present. Fasting was begun immediately on admission. On the first day there
was glycosuria of 10 gm. with excretion of 2.62 gm. total acetone. The plasma
showed sugar of 0.358 per cent, total acetone 14 mg. per 100 cc, CO2 capacity 64
per cent. Glycosuria ceased on the 2nd fast-day. Instead of a carbohydrate
period, a diet of meat, eggs, and thrice cooked vegetables was begun, at first
with only 20 gm. protein and 200 calories, but increasing to 40 gift, protein and
400 calories on Dec. 11. Fat was then added very gradually up to a maximum of
1450 calories on Feb. 6. The diet was then kept mostly at 1000 to 1350 calories,
but in Mar. by means of alcohol it was raised as high as 1650 calories. The con-
tinuous hyperglycemia and frequent glycosuria are shown by the graphic chart.
The patient was discharged Apr. 5, 1917, on a carbohydrate-free diet of 40 gm.
protein and 1000 calories, of which 350 were alcohol. The weight was 44 kg.
Edema being present, former weights of 41 to 42 kg. were probably more nearly
correct. The diet thus represented about 0.95 gm. protein and 24 calories per
kg., reduced by weekly fast-days to 0.82 gm. protein and 21 calories average.
The condition had been kept under partial control but the patient was not
benefited, for he was emaciated, weak, and neurasthenic, though still up and

396 CHAPTER III

about. He had also become discouraged. He continued treatment along the
above lines for several months at home, then gradually gave up the attempt to
remain sugar-free. He continued, however, to follow a low regulated diet, with
occasional fast-days to check progressive symptoms. Reports in the fall of 1917
indicated heavy glycosuria and acidosis and the certainty of early death.'

Remarks. — One fact stands beyond question; in a case of this type the func-
tional overstrain represented by continuous hyperglycemia and tendency to re-
current glycosuria is of itself sufficient to bring about relapse and downward
progress. Life was very much longer than in patients of similar type who aban-
don dietary restriction altogether. Whether any other cause of downward prog-
ress was present in this case is not known.

CASE NO. 57.

Male, married, age 37 yrs. American Jew; physician. Admitted Nov. 15,
1915.

Family History. — Grandparents all lived to healthy old age. No family disease
known up to this point. Patient's father and mother were first cousins. Father
still enjoys excellent health at age of 69. No taint on his side of family, except
death of a sister from carcinoma of stomach. Patient's mother died at age of 27
of diabetes. She was one of four children. One brother is well, another brother
has diabetes, a sister died a year ago of diabetes. The present patient was
the third of four children. The first died of imknown cause 1 year after birth,
the second is alive but highly neurotic, the fourth child is a sister stiU hving
but with severe diabetes. The entire family are moderately but not extremely
obese.

Past History. — Patient always strong, though somewhat obese. Measles at 8.
No sore throats or other childhood infections, but a few attacks of tonsillitis
since diabetes began. Even in childhood he had huge appetite and has always
eaten excessive quantities of sweets and desserts. No tobacco. No alcohol be-
yond one glass of beer daily. Eight cups of strong coffee every day. Has taken
relatively little exercise. Has slept well, but is of fairly nervous disposition. In
the 2nd year of medical school in 1899, he tested his urine in chemistry class,
and it contained sugar at that time. During his interne year he was yellow with
catarrhal jaimdice for about 8 weeks, but there was no fever or confinement t j bed
and no sign of any such trouble since. Always had tendency to profuse sweating,
but very marked hs^peridrosis began that year, and he has since been compelled
to use T^TT to ^^5 grain atropine occasionally to control sweating; has sometimes
taken it every day or two in summer. His weight before diabetes was 250
pounds, girth of waist 54 inches. He has been married 9 years; wife healthy,
but they have avoided pregnancy because of diabetes.

* Coma death occurred in Jan., 1918.

CASE RECORDS 397

Present Illness. — No attention was paid to the glycosuria found in 1899, and it
presumably continued. In 1907, losses during financial panic caused worry. An
attack of general furunculosis came on 2 weeks later, and glycosuria of 5.4 per
cent was then found. The diet was only moderately restricted; in particular
much oatmeal was allowed. Since that time he has almost never been free from
superficial infections, chiefly as boils on the neck; but any scratch or even a
chapped finger always takes a very long time to heal. In 1908, he received treat-
ment with oatmeal, codeine, and arsenic. Another physician subsequently ap-
plied the oatmeal treatment. Such treatment was also supervised by von Noor-
den on one of his visits to this country. In 1913, 10 months of lactic acid bacillus
treatment was tried under two of the chief advocates of this plan. Glycosuria
remained heavy through these years. There was no acidosis or loss of weight,
and the patient merely felt continually weak and run-down. In 1914, stricter
treatment was undertaken by still another diabetic specialist, who ordered a
measured diet, with 2 slices of toast as the only carbohydrate daily, and green
days twice a week. Later the toast was replaced by casoid biscuit. Even
with strict following of diet, heavy glycosuria persisted; but at times the patient
found the restrictions intolerable and consumed huge quantities of hot cakes and
maple syrup at restaurants. Last June there was another attack of general
furunculosis; four of the boils had to be incised. The patient was in bed 3 weeks,
and healing of the wounds required 3 months. His gums have been receding
and his teeth breaking. The very troublesome hyperidrosis and unbearable
sensations of heat in a warm atmosphere are one permanent complaint.

Physical Examination. — Height 170 cm. A healthy, comfortable looking,
florid faced, moderately obese man with sweaty skin. Numerous scars of healed
or nearly healed furuncles scattered over body. Teeth as described. Tonsils so
large that they block throat, crowding uvula up and leaving only a narrow sUt
between them, yet patient says that one slight attack of tonsillitis per year is
all the trouble they ever make. Several glands beneath jaw are enlarged to
hazel nut size. Blood pressure 120 systolic, 85 diastoHc. Knee jerks present but
diminished. Physical examination otherwise negative.

Treatment. — During 4 full days in hospital the patient was allowed to foUow his
appetite, with carbohydrate limited to green vegetables. Thus, on Nov. 17 to 19,
he ate 166 gm. protein, 30 to 40 gm. carbohydrate, and 4000 calories daily, and
excreted 16.7, 31.6, and 14.5 gm. sugar, with only slight ferric chloride reactions
and low normal plasma bicarbonate. 4 days of fasting were then imposed, a
trace of glycosuria remaining in the early hours of the last day. Without waiting
for full 24 hours of sugar-freedom, feeding with green vegetables was begun on
Nov. 24 and increased to 100 gm. carbohydrate on Nov. 26, when a trace of gly-
cosuria appeared. After a fast-day on Nov. 28, carbohydrate was begun in the
form of oatmeal, for comparison with the green vegetables. Glycosuria ap-
peared with 250 gm. carbohydrate on Dec. 5, and remained no more than a trace
with increase to 300 gm. carbohydrate on Dec. 6. The oatmeal being eaten
plain after 3 hours boiling, with no flavoring but salt, and nothing else being

398 CHAPTER m

permitted but 300 cc. coffee and 300 cc. clear soup, the caloric intake was thus
kept down to undernutrition level. After a fast-day on Dec. 7, another test was
begun with potato under the same conditions. 500 gm. carbohydrate were toler-
ated in this form, causing only a trace of glycosuria on Dec. 15, which cleared
up with the same intake on Dec. 16. The patient had been longing for potatoes
for many years, but the test was stopped because he could not eat a larger
quantity.

After a fast-day on Dec. 17, an attempt was made to compare the different
proteins in their effect upon the carbohydrate tolerance, potatoes being used
because the patient enjoyed them so much. On Dec. 18, glidine was given with
potato, but the test had to be broken off because the taste of glidine caused
nausea. Begioniag Dec. 19 the protein used was in the form of meat (beef,
veal, pork, every day). A trace of glycosuria thus appeared on Dec. 19 with
136 gm. meat-protein and 300 gm. potato-carbohydrate, and increased only
slightly with the increased intake of 150 gm. protein and 400 gm. carbohydrate
on Dec. 20 and 21. Instead of a fast-day on Dec. 22, 927 calories of fat were
given in the form of butter. The glycosuria cleared up in practically the same
manner as on plain fasting, a trace being present only in the early hours. The
ferric chloride reaction remained negative, notwithstanding the fears once enter-
tained concerning lower fatty acids in butter. , On Dec. 23, this same quantity of
butter fat was given with 100 gm. potato-carbohydrate, and glycosuria resulted,
in contrast to the far higher tolerance shown for potato without fat. On Dec. 24,
three eggs were added and the carbohydrate simultaneously increased to 200 gm.
On Dec. 25, 300 gm. potato-carbohydrate with 100 gm. butter iat without eggs
resulted in still heavier glycosuria. Protein starvation was continued on Dec.
26 and 27, 400 gm. potato-carbohydrate being given daily with 100 gm. butter
fat. Moderately heavy glycosuria was continuous, showing a well marked re-
duction of tolerance by fat as compared with the former period of potato alone.
A fast-day on Dec. 28 stopped the glycosuria.

Beginning Dec. 29, the desired test with vegetable protein was made by the
use of Barker's gluten flour. Glycosuria appeared on the first day with 124 gm.
protein and 204 gm. potato-carbohydrate. It became constantly heavier as the
intake was raised to 148 gm. protein and 404 gm. carbohydrate. No appreci-
able advantage of vegetable protein, therefore, was perceptible in comparison
with the previous period of potato and meat. After stopping the glycosuria by
the fast-day of Jan. 2, green vegetables were resumed. On accoimt of the quan-
tities of carbohydrate, it was necessary to include the higher classes up to green
peas, green lima beans, beets, tunups, etc. Faint or doubtful traces of glycosuria
were present on each day, but did not increase as the intake was increased from
200 to 400 gm. carbohydrate in this form. Therefore, no special superiority of the
form or kind of carbohydrate was definitely demonstrable between oatmeal, pota-
toes, and green vegetables, variations of the patient's tolerance being sufficient to
account for the facts observed.

CASE RECORDS 399

This patient was one of several diabetics discharged rather hastily because of
an epidemic of grippe in the hospital. Jan. 8 to 10 his diet was rapidly built up
to 150 gm. protein, SO gm. carbohydrate, and 3000 calories. The reduction of
copper shown amounted to only doubtful traces in a single voiding each day, and
was judged to be due to a concentrated urine, not true glycosuria. The patient
had recovered complete health, such as he had never enjoyed during the time of
his diabetes, and left to undertake active medical work. Hyperidrosis had ceased,
along with the other symptoms.

Acidosis. — The slight degree of acidosis after so many years of heavy glycosuria
was one of the indications that this was essentially a mild case, though the patient
and all who had treated him regarded it as severe and intractable. The specific
difference as respects acidosis seems to be illustrated by comparison of this patient
with others in the series. Not only was this patient rather obese, but also on Nov.
18, for example, he ingested only 37.7 gm. carbohydrate in the form of green
vegetables (presumably not all absorbed) and excreted 31.6 gm. sugar. The rest
of the diet consisted of 166 gm. protein and 344 gm. fat. Yet this large quantity
of fat was disposed of with such slight traces of ketonuria that quantitative esti-
mation was considered not worth while. The plasma bicarbonate likewise remained
within normal limits. There was a slight fall in CO2 capacity in the initial fast,
but no serious acidosis was shown either by this or the clinical symptoms, though
the ferric chloride test became heavy. It is noteworthy that distinct ketonuria
continued during the period up to Dec. 7, when the patient was receiving absolutely
no food but oatmeal, in quantities increasing from 25 up to 300 gm. carbohydrate.
Even large quantities of assimilated carbohydrate therefore did not necessarily
clear up ketonuria promptly and completely.

Blood Sugar. — This gave another indication of the inherent mildness of the
case. Hjrperglycemia between 0.25 and 0.3 per cent, as shown at admission, had
presumably been present for a number of years. It was remarkable that it should
have fallen to normal so quickly. The marked hyperglycemia with sUght glyco-
suria dming the subsequent carbohydrate tests indicated a high renal threshold.
Fast-days brought the sugar promptly to normal.

Carbohydrate "Cures." — The diabetes here was so stubborn that it had for
years resisted oatmeal "cures," "green days," and restricted diet, under the
care of consultants experienced in the management of diabetes. The case was
a typical example of so called "protein sensitiveness," "fat sensitiveness," and
"paradoxical tolerance." The first two terms have been used to denote suscepti-
bility to glycosuria from the addition of protein or fat to a standard diet. The
last is NaunjTi's expression for cases with glycosuria continuously present, but
showing little diminution of glycosmia on diminishing carbohydrate and little
increase upon addition of even considerable quantities. These peculiarities were
all illustrated in the above tests. The actual condition was a mild diabetes with
obesity. Under the prevalent misconception that obesity in itself is a favorable
feature, this patient had been restricted in carbohydrate, but continuously
"built up" with protein and fat, and the intractable glycosuria was due to this

CASE RECORDS 401

War Demonstration Hospital of this Institute on Jan. 21, 1918, for Carrel-Dakin
treatment or amputation if necessary. Immediate fasting changed the condition
so promptly that surgery was unnecessary, and rapid healing without deformity
resulted. On Feb. 2, the patient was able to leave, free from hyperglycemia as
well as glycosuria and acidosis, to finish convalescence at home. The lesson has
been effective, and he has returned to the condition stated after his first discharge.
Remarks.— The record illustrates what can be hoped for in a large proportion
of cases not of such maximal severity as those comprising the majority of this
series; it further illustrates the dangers of excessive diet and weight even in
patients of this type.

CASE NO. 58.

Female, married, age 72 yrs. American. Admitted Dec. 3, 1915.

Family History. — No heritable disease.

Past History. — Very healthy life under excellent hygienic conditions. Whoop-
ing-cough in childhood the only infection remembered. "Never sick a day."
Never any throat or tonsil trouble. Eyes have always been weak. Teeth all
removed within the past decade. Married 55 years. One still-birth; one child
died in infancy; five children are well. Habits regular, appetite moderate. No
excesses of any description.

Present Illness. — 4i years ago patient consulted an oculist for failing vision.
Diabetic retinitis was diagnosed, and the oculist advised that efficient treatment
■ of the diabetes was necessary in order to save her eyes. Physicians have em-
. ployed half-hearted measures, and she has never been free from glycosuria. There
has been polydipsia and pol3ruria, but no polyphagia. Vision has grown pro-
gressively worse, and the patient came to the Institute on this account.

Physical Examination. — Height 155 cm. Normal development, slight obesity.
Skin very dry. Blood pressure 185 systolic, 120 diastolic. Teeth false. Slight
emphysema. Liver edge palpable 4 cm. beneath costal margin. Examination
by oculist showed double senile unripe cataract preventing retinal examina-
tion; amblyopia with inability to count fingers at 2 meters. Over internal mal-
leolus of left foot is an encrusted, red and angry-looking, but painless sore about 2
cm. in diameter. Scabs showing less inflammation are present over the meta-
tarsal joint of the great toe and on the dorsum of the third toe of the same foot.
Examination otherwise negative.

Treatment. — The 1st full day in hospital, a diet was given of 99 gni. protein,
15 gm. carbohydrate, and 1900 calories. The urine showed 26.65 gm. sugar,
and the ferric chloride reaction, which had been negative, became sUght during
this day. It then became apparent why physicians had failed to check the gly-
cosuria, notwithstanding the ocular damage; for when carbohydrate was entirely
withdrawn and the total diet reduced to 75 gm. protein and 1600 calories, glyco-
suria diminished slightly but remained rather heavy, and the ferric chloride reac-
tion became moderately heavy. Accordingly, after a week of such diet, 2 days
of fasting (Dec. 11 and 12) were given. Glycosuria ceased, but a moderate ferric

402 CHAPTER in

chloride reaction continued. The usual green vegetables were then begun with
10 gm. carbohydrate on Dec. 13 and increased rapidly, until glycosuria appeared
with 100 gm. on Dec. 16. The ferric chloride reaction consequently became
negative. The diet was then rapidly built up to 70 gm. protein and 1500 calories,
the urine remaining normal. The patient was discharged Dec. 24. The dry skin,
patches of threatened gangrene, and other minor conditions had cleared up, and
the patient stated she felt better than for years past.

Acidosis. — There was never any clinical symptom of acidosis. The develop-
ment of rather marked ferric chloride reactions in a mild case of diabetes when
the diet is restricted, has frequently, as in this instance, frightened physicians so
that they refrained from taking the measures imperatively demanded to control
such a genuinely serious compUcation as diabetic retinitis. On the other hand,
if this warning sign were entirely ignored and a high protein-fat ration kept up,
it might readily bring on coma even in some patients with mild diabetes.

Blood Sugar. — On the day of discharge with normal urine, the sugar was still
0.147 per cent in whole blood and 0.175 per cent in plasma. In view of the pa-
tient's age, the mildness of the case, and the expectation of improvement with
time, this hyperglycemia required no more rigorous measures for the immediate
present.

Weight and Nutrition. — ^The weight at admission was 68 kg., at discharge 67.2
kg. The diet prescribed at discharge was 70 gm. protein, 15 gm. carbohydrate,
and 1500 calories (a little over 1 gm. protein and 22 calories per kg.). Mild
exercise suitable to her age was advised, and a continuance of sb'ght undernu-
trition was desired, while the cataracts were ripening.

Subsequent History. — The patient remained sugar-free, aside from a few traces
due to slight laxity in the care of an indulgent daughter. The diet was sufficiently
bulky and entirely satisfied the patient, except that she still entertained some
longing for the desserts of the past. She was readmitted to the hospital June 8,
1916 for cataract operation.

Second Admission. — The weight was now down to 62.6 kg., the urine normal,
and the strength at its best. The prescribed diet was continued. On June 10,
sugar was 0.145 per cent in both whole blood and plasma. By June 26 it had
further diminished to 0.111 per cent in whole blood and 0.128 per cent in plasma,
although the carbohydrate meanwhile had been increased to 30 gm. Tests showed
that 50 gm. carbohydrate could be tolerated, but instead of maintaining this in-
take, 30 gm. carbohydrate were resxmied and the protein increased to 90 gm. Cata-
ract operation was performed on July 11 without glycosuria, acidosis, or any
untoward incident. Diabetic retinitis was diagnosed thereafter. The patient
was discharged July 28. The weight was now down to 59 kg., which was suffi-
cient for her figure, and the health was stiU further improved-.

Subsequent History. — ^After several months of sugar-freedom and favorable
progress, she began to steal sweet and starchy foods, and reached a chronically
weak condition with continuous glycosuria. Gangrene of the foot then necessi-
tated fasting, which was conducted at home, and sugar-freedom has since been

CASE RECORDS 403

maintained on restricted diet. At last report (1918) glycosuria was absent, but
owing to two apoplectic strokes and an intestinal obstruction diagnosed as car-
cinomatous, death was expected within a few weeks or months.

Remarks. — Diabetes at such an age is usually easy to control. The very high
proportion of senile patients who sooner or later lose comfort and even life by
reason of gangrene or ocular or other complications indicates the error and danger
of the widespread belief that glycosuria at this age is harmless enough to be
neglected. Efficient treatment is indicated, for relief, if complications are present,
and for prophylaxis if they are not present. The general health as a rule is
improved, and it becomes evident that part of the trouble attributed to senility
was due to diabetes. Surgical operations should then be performed if required.

CASE NO. 59.

Male, married, age 46 yrs. American; physician. Admitted Dec. 29, 1915.

Family History. — Father died supposedly of cancer of Uver at 64 years, but there
are indications that the condition may have been luetic. Mother is living, aged
83, and has rheumatism and gout. A maternal aunt died of diabetes. One
brother of patient is well. One sister died after an acute illness of 3 days in some
form of coma, apparently following tonsillitis; there was a history of increasing
attacks of so called "acidosis" preceding, partially relieved each time by alkali;
there was also the possibility of slight h3?perth3T:oidism. Patient has been mar-
ried 8 years; wife and one 6| year child are well; another child died a year ago
with lymphatic leucemia and Streptococcus hatmlyticus infection.

Past History. — Measles, whooping-cough, and probably scarlet fever before 10.
Tendency to biliousness, nausea, and vomiting throughout childhood. One severe
sunstroke in boyhood. Patient was always rather frail in physique, of nervous
type, addicted to overwork. He blames overwork in college, financial worries,
and subsequent professional strain for his condition. In 1899 he was refused life
insxurance because of albuminuria with casts. Subsequently, with some difficulty,
he obtained a policy. Little alcohol; 10 to 15 cigarettes daily. No excesses in
diet or carbohydrate. There was a period beginning in 1889 when diabetes may
have been present unknown. There was persistent sciatica for the year 1889 to
1890. He has suffered for many years from true t)rpical gout. There were numer-
ous attacks in 1900, but the gout has diminished since 1907. In 1894, he under-
went an operation for axiRary abscess following a finger infection. In 1896, he
had numerous boils and carbuncles, treated by incisions and vaccines.

Present Illness. — ^The diagnosis of diabetes was not made until 1910, when
poljfiuia began. Treatment has been interfered with by professional duties, and
owing to downward progress the patient visited a specialist 2 years ago. He was
made sugar-free and his weight reduced from 137 poimds to 120| pounds. Upon
returning to New York he resumed his attempt to carry heavy professional work
and keep his diabetes secret. This necessitated violations of diet when attend-
ing dinners in company, so that relapse resulted. He came to the Institute
because he had finally lost power to continue his work.

404 CHAPTER in

Physical Exammation.— Height 1 76 cm. Normal development, decided emacia-
tion, marked weakness, but no acute symptoms. Slight diarrhea. Lymph
glands generally palpable. Blood pressure 118 systolic, 88 diastolic. Knee jerks
just obtainable with reinforcement. Wassermann negative. Examination other-
wise negative.

Treatment. — For 3 days the patient was kept on an observation diet of 76 gm.
protein, 10 gm. carbohydrate, and 2100 calories, about 200 calories being whisky.
The glycosuria of 0.88 per cent on the first day diminished to a trace by the third
day, and then ceased with 1 day of fasting. The ferric chloride reaction cleared
up in parallel. A carbohydrate test in the usual form showed a tolerance of 90
gm. carbohydrate, glycosuria resulting from 100 gm. on Jan. 10 to 11. A mixed
diet was then built up, containing 20 gm. carbohydrate and 1900 to 2400 calories.
The patient contracted a mild but persistent grippe infection, which was largely
responsible for the frequent traces of glycosuria. Beginning Feb. 18, the calories
were diminished to 1900. The grippe passed off and the tolerance improved, so
that at the end 90 gm. protein, 50 gm. carbohydrate, and 2245 calories were
taken without glycosuria. He was discharged Mar. 16 feeling improved, but
still below normal strength.

Acidosis. — The ferric chloride reaction jpromptly became negative. The CO2
capacity was practically normal throughout. In the initial fast it fell from a
high to a low normal, and it at first tended to be down after fast-days. The
tendency to a slightly high ammonia excretion was the only evidence of acidosis.

Blood Sugar. — Marked hyperglycemia present at admission was rather promptly
brought to normal. Subsequently the figures were generally normal after fast-
days, but showed hjrperglycemia on other days. Grippe was partly responsible,
but the marked h3rperglycemia, particularly at the close, was clear evidence that
the diet was too high.

Weight and Nutrition. — The weight at admission was 52.6 kg., at discharge
50.4 kg.; i.e., a loss of 2.2 kg. The above mentioned diet at discharge thus rep-
resented 1.78 gm. protein and 44.6 calories per kg., reduced by the weeklyfast-
days to about 1.5 gm. protein and 38 calories per kg. The body weight in this
calculation was a very low one; nevertheless the condition was obviously not
under good control, and therefore such a liberal diet was a mistake.

Subsequent History. — The patient went to the seashore to rest under favorable
conditions. In the 2 weeks between discharge and Apr., he gained 4J pounds
and showed glycosuria 9 times, a slight cold being blamed for part of the trouble.
The diet was then changed to 127 gm. protein, 35 gm. carbohydrate, and 1950
calories. On this, glycosuria was almost continuously absent. He tried to
build himself up with exercise in the form of goU, but in the middle of Apr. devel-
oped a slight infection and herpes zoster. He then rettmied to New York, where
his diet could be more closely supervised, and the ration was reduced to 75 gm.
protein, 10 gm. carbohydrate, and 1900 calories. On this, glycosuria was almost
continuously absent; but in Jime another cold occurred with sinus infection, so
that traces of glycosuria were present almost continuously June 5 to 20. Twelve

CASE RECORDS 405

blood analyses between Apr. 28 and June 12 showed continuous hyperglycemia
and normal CO2 capacity, the lowest plasma sugar being 0.135 per cent, the
highest 0.218 per cent, and the average 0.177 per cent. Because of the unfavor-
able progress, the patient was readmitted June 20, 1916.

Second Admission. — The weight was 52.2 kg., as against 50.4 kg. at discharge
and 52.6 kg. at the first admission. The strength and spirits were decidedly
improved as compared with the first admission. On June 21, the glycosuria was
6.7 gm., the CO2 capacity 56.1 per cent, the sugar in whole blood 0.228 per cent
and in plasma 0.244 per cent. The diet was kept up to the maximmn prescribed
outside the hospital, and no fast-days were imposed. Traces of glycosuria were
present frequently on 2100 to 2250 calories, but for 3 days at the close (July 10
to 12), 90 gm. protein, 15 gm. carbohydrate, and 2000 calories were taken without
glycosuria. The patient's strength had improved so that he was able to go on with
moderate professional work. The weight was tmchanged during this period in
hospital. The hyperglycemia also showed practically no change. The renal
threshold for sugar was evidently high, but the urea index on June 28 was deter-
mined by Dr. Palmer as 200; also (the patient frequently worrying over his gouty
history) the uric acid in the blood was 2.8 mg. per 100 cc.

Subsequent History. — The patient went to a country place and attempted to
build up his physical condition by exercise and general care, but never succeeded
in regaining strength or working capacity. He had trouble with nausea, edema,
and mental irritability and depression, partly due to trouble with a tooth. Gly-
cosuria was almost continuously absent.

Third Admission. — July 31 the patient was readmitted to undertake a some-
what more thorough treatment. His intense desire to go on with active profes-
sional work had been a hindrance to radical measures. With glycosuria and keto-
nuria absent, the sugar was 0.200 per cent in whole blood, 0.208 per cent in plasma,
CO2 capacity 52.8 per cent. The output of ammonia nitrogen was 0.76 gm.jof
acid (Folin) 468 cc. 0.1 n. The weight was 52.5 kg.; i.e., practically the same as
at first admission. After 3 days on the prescribed diet, a fast-day was given on
Aug. 4, followed by a carbohydrate tolerance test. A trace of glycosuria appeared
Aug. 17 to 18 with 130 gm. carbohydrate. The tolerance of 120 gm. thus seems
to indicate an increase of 25 per cent over the first test in Jan. He was then
put back on a mixed diet of 90 gm. protein, 15 gm. carbohydrate, and 2000 cal-
ories, and was discharged on this Aug. 24. The weight had been reduced to 50
kg., and the blood sugar to 0.143-0.185 per cent. There had been another slight
gain in general health and spirits.

Subsequent History. — The patient went to the Catskills for the summer and to
California for the winter. On accoimt of recurrence of glycosuria, his diet has
had to be again reduced to 75 gm. protein, 10 gm. carbohydrate, and 1900 calories.
He remains a fairly comfortable semi-invalid, stronger and better in all respects
than at first admission, and hoping to return to work if he can improve a little
more.

406 CHAPTER III

Remarks.— A number of these patients have been tried on what could be callec
a modified Naunyn treatment; that is, using more or less prolonged fasting anc
perhaps transitory reduction of weight to suppress glycosuria, and then giving thi
maximal diet possible in order to keep up a maximum of weight and strength. I:
the diabetes has any claim to be called severe, the results of such a method an
imiformly and necessarily bad. In view of this patient's age, some power o;
recuperation may be expected. There is a possibility that slight improvement
may occur, as indicated by the higher tolerance in the carbohydrate test in spit(
of the excessive diet, the case somewhat resembling the milder ones in oldei
persons. It is more probable that a case of this severity will sooner or latei
show downward progress, which may be called "spontaneous," but is sufficientlj
accounted for by inadequate treatment. The persistent marked hyperglycemia
not tending to improve, and the slight acidosis indicated by a slightly elevated
ammonia output, are plain evidence that overstrain of the weakened function has
been only diminished and not stopped, and unless there is an unexpectedly high
spontaneous recuperative power, the downward progress will be merely slowed, not
stopped. The high diets in this and other patients do not even serve the intended
purpose of keeping up weight, strength, and resistance, for these poorly treated
patients are the very ones who are most subject to infections and suffer most
harm from them.

The patient's ambition of resuming active work has not been achieved. He
would doubtless be far nearer to it, and in better condition in all respects, if he
had at the outset been brought down to a suitably low level of diet and weight.
A lower level of weight, efficiency, and comfort than required in such a plan will
probably result here, as it has in other cases, from the gradual downward prog-
ress, and this loss of weight will be attended not by benefit but serious injiu-y
of the assimilative function. Thorough treatment should still offer much hope.

CASE NO. 60.

Female, married, age 43 yrs. American; housewife. Admitted Jan. 1, 1916

Family History. — Parents lived to old age. Two brothers and one sister well.
Husband and one 6 year old child well. No other pregnancies. No diabetes or
other heritable disease known in family.

Past History. — Very healthy life. Whooping-cough, measles, and chicken-pox
in childhood. "Gastric fever" in 1896; in bed 3 or 4 weeks. Frequent attacks
of tonsillitis up to 10 years ago, none since. No other illnesses. Appetite, diges-
tion, bowels, menstruation, and sleep normal. Never nervous. No excesses of
any kind.

Present Illness. — About 9 months before admission, patient noticed that she
was losing weight and was imduly thirsty. After 2 months (June, 1915) a physi-
cian consulted for pruritus vulvae diagnosed diabetes. The patient was fasted
for a day or two, then placed on a diet of eggs and milk. She was said to be
"practically sugar-free," but continued to lose weight and strength. In Aug.

CASE RECORDS 407

1915, she came under the care of a speciah'st for 6 weeks, first in hospital and sub-
sequently at home. She was made sugar-free by fasting, and then kept on a mmi-
mal diet. She lost 60 pounds weight, and was referred to the Institute as a Case
of extremely severe diabetes. .

Physical Examination. — Height 153.8 cm. A very emaciated woman, with fair
strength and no acute symptoms. Slight hyperpnea and drowsiness are present,
but are probably accounted for largely by weakness and weariness after -her
railroad trip. Teeth in good condition. Tonsils hypertrophied. Breath has
acetone odor. Knee jerks not obtainable even with reinforcement. Wasser-
mann negative. Examination otherwise negative.

Treatment. — On Jan. 1, the day of admission, the patient received 54 gm. pro-
tein, 5 gm. carbohydrate, and 1247 calories, and excreted 20.4 gm. glucose, 1.6
gm. amnjonia nitrogen, and 495 cc. 0.1 n acid, with an intense ferric chloride re-
action. 3 days fasting was then imposed, with resulting glycosuria of 11 gm. on
Jan. 2, 9.2 gm. on Jan. 3, 12.1 gm. on Jan. 4. As the weakness seemed to be of
dangerous degree, the tempting experiment was tried of feeding a liberal diet in
the hope of getting a fresh start for subsequent fasting. Accordingly, on Jan. S,
2 eggs were given, with coffee and clear soup each 300 cc. as during fasting.
The diet was rapidly built up (Jan. 6 to 11) as high as 75 gm. protein and 2150
calories on Jan. 10. Glycosuria increased only to 24.1 gm., but hyperpnea,
drowsiness, and nausea developed. The plasma bicarbonate fell sharply to 24.6
per cent, while the ammonia nitrogen rose to 3.19 gm., with urinary acidity of
335 cc. 0.1 N. Fasting had to be resumed to ward off coma, with the patient
worse instead of better than before. Under fasting without alkali, the above
mentioned low CO2 on the morning of Jan. 12 rose to 27.6 per cent by evening of
the same day. Thereafter it cUmbed steadily, and the patient was out of danger
within 24 horns. On Jan. 14, 2 and on Jan. 15, 3 eggs were allowed in addition
to soup and coffee. After a plain fast-day on Jan. 16, 420 calories of whisky
daily were begun, 1 egg also being allowed on Jan. 17. Glycosuria had been
diminishing, and cleared up on Jan. 19. After about 40 hours of sugar-freedom,
10 gm. carbohydrate in the form of green vegetables were given on Jan. 21, and
20 gm. on Jan. 22. Slight glycosuria resulted, and persisted as the carbohydrate
intake was increased as high as 35 gm. on the following days. After a fast-day
with 150 cc. whisky, 400 gm. thrice boiled vegetables, and 60 gm. bran biscuit
on Jan. 28, a very low carbohydrate-free diet was attempted. On Feb. 5, when
this had been built up to 50 gm. protein, 850 calories (245 being alcohol), and 300
gm. thrice boiled vegetables, a trace of glycosuria appeared, requiring a fast-day
on Feb. 6. With the same number of calories, and diminution of protein to 40
to 35 gm., glycosuria continued. It still persisted with 12.5 gm. protem and 450
calories (315 being alcohol) on Feb. 10, and a fast-day on Feb. 11 was necessary
to abolish it. Beginning Feb. 12, the diet was again cautiously built up to 42
gm. protein and 650 calories (315 being alcohol). Glycosuria on Feb. 17 and 19
required a fast-day on Feb. 20. With the same calories and reduction of protein
to 35 gm., glycosuria still recurred, requiring another fast-day on Feb. 27. A

410

CHAPTER III

in whole blood and 0.333 per cent in plasma on Jan. IS. A faU then began, and
on Jan. 25, on alcohol and green vegetables, the sugar was down to 0.143 per
cent in whole blood and 0.167 per cent in plasma. The values then began to
approach normal, and from Mar. 7 to 29 it can be said that vmdemutrition had
brought about normal blood sugar as judged by morning samples before breakfast.
The subsequent higher diets brought back hyperglycemia, which was reduced by
the lower diet beginning Jxme 3. Increased diet again brought a rise on June
23, but on Jime 28, on the diet proposed for discharge, the blood sugar was be-
low 0.15 per cent, which seemed rather satisfactory in such a case at this stage.
Weight and Nutrition. — For 5 months before admission the patient had been
extremely undernourished, green vegetables up to or slightly past the Umit of toler-
ance, and a few eggs, having been almost the only nourishment in this time.
This had repressed the dangerous acidosis to the greatest possible degree, but
both body fat and body protein had necessarily been sacrificed heavily in the
process. The process had been persisted in, though the patient felt fairly well
and strong at the outset in Aug., and on admission in Jan. was emaciated and
seriously exhausted. Accordingly, the experiment was tried of feeding more
liberally for a short time in the attempt to restore some strength, so as to get a
fresh start for further fasting. Though the diets on Jan. 5 to 11 averaged only
33 calories per kg. of body weight, the attempt caused only harm ipstead of bene-
fit, as always in genuinely severe cases. The question thereafter was whether the
glycosuria could be controlled without starving the patient to death. The method
used consisted in alcohol short of any perceptible symptoms, protein generally
on feeding days above 1 gm. per kg. of weight, and close restriction of fat, so
as to maintain almost continuous undernutrition. It would doubtless have been
better if alcohol had been omitted and the fat had been excluded stDl further,
and the condition thus controlled earlier and more radically. The weight at ad-
mission was 36.6 kg. The gain in weight about Feb. was due to edema, which
was controlled by regulation of the salt intake, sodium chloride being given,
weighed Uke the rest of the diet, first 10 gm. and later 8 gm. daily. The weight
at discharge was 33 kg.; i.e., a loss of 3.6 kg. The low level of metabolism caused
by undernutrition is thus illustrated, for a patient starting well nourished at the
outset would have lost much more weight on such a diet. The degree of imder-
nutrition is shown in the following calculation.*

183 days.

Alcohol calories 55,496

Food " 81,878

Total " 137,374

Protein 5,162 .3 gm.

Fat 6,109.9 "

0.83 gm.
0.98 "

The diet prescribed at discharge was 50 gm. protein and 1000 calories, more
than a third being in the form of alcohol as shown, (1.5 gm. protein and 33

CASE RECORDS 411

calories per kg., reduced by partial fast-days to about 1.4 gm. protein and 31
calories per kg.).

Subsequent History. — The patient was discharged with the idea that she might
be able by great care to remain 2 or 3 weeks at home. She was actually at home
4 months and 1 week, remaining free from glycosuria, except for traces on a very
few days, on account of which the diet was ordered on Aug. 16 to be reduced to
40 gm. protein and 800 calories. She was readmitted for further treatment Nov.
8,1916.

Second Admission.— Weight 29.9 kg.; i.e., a loss of 3.1 kg. since discharge.
In addition to glycosuria, a slight ferric chloride reaction was present. Instead
of fasting immediately, the diet was limited to green vegetables representing 20
gm. carbohydrate, and diminishing to 5 gm. carbohydrate on Nov. 12. 2 fast-
days, Nov. 13 and 14, left the urine normal. On Nov. 15, 5 gm. carbohydrate in
the form of green vegetables were assimilated, but 10 gm. on Nov. 16 brought a
trace of glycosuria. Carbohydrate-free diet was then built up, beginning with
1 egg and 360 calories on Nov. 17, and increasing to 6 eggs and 1200 calories on
Nov. 22. Continuance of this diet brought glycosuria beginning Nov. 25, re-
quiring a fast-day on Nov. 27. Thereafter similar diets (40 to 50 gm. protein and
1150 to 1300 calories) were continued, with routine weekly fast-days. The effect
of these in checking acidosis is shown by the ammonia curve. No more than the
faintest traces of glycosuria appeared, but these were unduly frequent. Though
the food was thus pushed to the utmost limit of tolerance, it was not possible to
prevent gradual loss of weight.

Lipemia was not noticed at the first admission. It was heavy at the second
admission, and gradually disappeared during the first week of treatment. The
difference may be attributed to the fact that the patient was eating little but
green vegetables when first received, but preceding the second admission had been
on protein-fat diet. No quantitative estimations were made.

The patient was dismissed Apr. 6, 1917, weighing 27.6 kg. The prescribed
diet represented 1.45 gm. protein and 45 calories per kg., reduced by the weekly
fast-days to 1.25 gm. protein and 39 calories average. The diet therefore was
absolutely very low. It appeared relatively high on account of the emaciation,
but either because of the relative increase in body surface, or the lack of carbo-
hydrate, or a specific diabetic disorder, it did not produce gain in weight.

Subsequent History. — The patient has since remained at home on the same
program as in hospital. She adheres rigidly to her diet and clears up traces of
glycosuria promptly by fast-days. There is little perceptible change up to the
present in weight, strength, or assimilative power.

Remarks. — By extreme undernutrition it has been possible to keep this patient
alive over 2 years from her first fasting treatment. Though always hungry,
excessively emaciated, and lacking strength for any real exertion, some of the
noteworthy feature? are her constant cheerfulness, freedom from infection, and
comfort in all other respects. She is able to be up and about, carries on light
household duties, and — the point of most importance to her — attends to the

414 CHAPTER III

sponse to slight dietary restrictions indicates no special difficulty in bringing
down the blood sugar. Nevertheless, the renal impairment served as a block to
the ordinary glycosuria, and the finding of as much as 0.73 per cent blood sugar
with only slight glycosuria shows the necessity of blood examinations in such
circumstances. The treatment was not so rigid as would be advisable if the
duration of hfe from other causes were less limited. On the other hand, to ignore
the diabetes would probably lead to aggravation of the entire condition and
materially shorten life.

CASE NO. 62.

Female, unmarried, age 19 yrs. American; houseworker. Admitted Feb.
19, 1916.

Family History. — Father, mother, one brother and two sisters are well. One
brother died in infancy of "spinal meningitis." A maternal grandmother died
of tuberculosis. No diabetes or other heritable disease known in family.

Past History. — Whooping-cough, measles, and chicken-pox in infancy. No
throat trouble. Grippe once. There is a hazy description of what the doctors
are said to have called diabetes at the age of 7. The symptoms are described as
puffiness of the face in the mornings, whiteness of the skin, and urine which
looked bloody and contained a heavy sediment. There was also skin eruption
over the back and legs described as "poison water blisters," which were small,
not hemorrhagic, and healed without scars. Treatment is said to have been by
diet with prohibition of starches. This trouble passed off after about a year.
The habits, appetite, digestion, bowels, and menstruation have been normal.
No alcohol. Moderation in tea, coffee, and carbohydrates. Not neurotic.
Always slept well and was imder no strain.

Present Illness. — Polydipsia and polyuria began in the summer of 1911. Dia-
betes was promptly diagnosed, and the diet was limited to proteins and fats with
vegetables. Glycosuria has been continuous since the beginning. Menstrua-
tion stopped 1 year after onset of diabetes, and bowels have become irregular.
There have been no infections or distressing symptoms. The patient has felt
reasonably comfortable while losing 30 pounds weight and corresponding strength.
Recently she noticed sKght edema of ankles and dyspnea on exertion. She applied
for treatment merely on account of knowledge that her condition was serious,
and not for any special urgent symptoms.

Physical Examination. — Height 157.5 cm. Mediimi development, rather
marked emadation. Skin dry. Cheeks flushed. Tongue red, teeth poorly
kept, two carious. Examination by specialist showed nose and ears normal;
no adenoids; tonsils sUghtly enlarged, showing a little thick yellow material on
pressure. Very sUght glandidar enlargement. Reflexes normal. Moderate
edema below knees. Examination otherwise negative. Wassermann negative.

Treatment. — On an observation diet of 75 gm. protein, 100 gm. carbohydrate,
and 2000 calories, there was excretion of 145.5 to 131 gm. glucose and 5.3 to 4.5
gm. ammonia nitrogen with intense ferric chloride reaction. On Feb. 25 and 26

416 CHAPTER m

Weight and Nutritiofi.— Weight at admission 39.4 kg., at discharge 36 kg.;
i.e., a loss of 3.4 kg. The lowest weight was 34 kg. on Mar. 20, following the
most extensive undernutrition. Some fluctuations in the weight cwrve were caused
by slight edema. The diet prescribed at discharge represented nearly 1.4 gm.
protem and 42 calories per kg., reduced by the weekly fast-days to 1.2 gm. pro-
tein and 36 calories average. Notwithstanding the loss of weight there had been
improvement in strength and comfort, and the patient was now walking 3 miles
daily and otherwise exercising without weariness.

Subsequent History. — On June 19, the plasma sugar was 0.161 per cent, CO2
capacity 52 per cent. June 30, sugar 0.156 per cent in whole blood, 0.172 per cent
in plasma, CO2 capacity 63.6 per cent. The weight was still 36 kg. Strength
had greatly increased, and the only complaint was of hunger. The urine had
remained consistently normal. The diet was increased to 60 gm. protein and
1550 calories. Glycosuria remained absent imtU Nov., and the general condi-
tion was excellent. Readmission was necessary Dec. 8, 1916, because glycosuria
was then persistent.

Second Admission. — Weight 37.2 kg., without perceptible edema. General
condition good. Acidosis was shown only by the heavy ferric chloride re-
actions and the ammonia nitrogen of 1 gm. Instead of immediate fasting.
Dr. Joshn's plan of a low fat-free diet was used. Thus, the diet on Dec. 9 con-
sisted of lean meat and green vegetables, representing 40 gm. protein, 20 gm.
carbohydrate, 10 gm. fat, and 336 calories. With gradual diminution of this diet
to 20 gm. carbohydrate and 9 gm. protein on Dec. 16, the ferric chloride reaction
became negative, the ammonia fell to 0.74 gm. N, and glycosuria diminished to
traces. It is noteworthy also that the total nitrogen excretion at first was 13
gm. daUy. This progressively diminished on the semifasting to the low figures
of 4.71 gm. on Dec. 14, 4.76 gm. on Dec. 15, and 4.37 gm. on Dec. 16. A single
fast-day on Dec. 17 cleared up the lingering traces of sugar. To protect body pro-
tein, 40 gm. protein daily were itmnediately given, without carbohydrate, and
with fat so strictly limited that the total calories amounted to only 600. The
patient was dismissed temporarily on this diet on Dec. 22, 1916, to be home for
the Christmas hohdays. Weight 34.4 kg.; strength and spirits good.

Third Admission. — ^Jan. 8, 1917. Patient returned according to arrangement, -
saying that she had enjoyed the holidays greatly. Weight 34.3 kg. Very slight
edema of legs. The diet remained at 40 gm. protein and 600 calories.

On Jan. 11, sore throat was complained of, but temperature was normal. On
Jan. 12, the temperature rose as high as 100.6°. On Jan. 13;'>it was not above
100°. On Jan. 14, the weight was 32.2 kg., and the temperature up to 103.4°.
There were signs of tj^jical pneumonia of right lower lobe; sputimi showed Type
IV pneumococcus; blood cidture negative.

The conditions during this attack of typical lobar pneumonia in a severely
diabetic patient are best shown m Table XVII. No alkali was employed.

Beginning Feb. 3, the protein was increased to 40 gm. daily. Thereafter the
total calories were gradually increased to 900. Beginnmg Feb. 10, the protein

CASE

RECORDS

417

TABLE XVII.

ate.

S

Diet.

.a

Urine.

Blood
plasma.

r

1

1

It

"o

II

.

£i ^

iz;

1

8

1917
Jan. 13

is.
32.6

'F.

94.4
100. C

gm.
4.3

em.

gm.
10

gm

61

cc.
2100

cc.

2547

0

0

gm.
0.8C

ter
cent

—

vol.
ter
cent

a

14

32.2

102.0
103.4

8.6

0.9

20

—

125

3562

3017

+

0

0.57

—

—

It

15

32.3

104.2
103.5

18.3

10.9

8.2

—

209

3800

2265+

+

0

0.70

0.268

68

tt

16

32.1

103.8
101.6

22.3

15.9

—

—

240

3025

3238

+

+

0.83

—

—

it

17

31.7

104.0
102.0

22.3

15.9

—

—

240

3700

2943

+ .

+

1.26

0.227

60

ft

18

31.8

102.8
100.6

22.3

15.9

—

—

240

3900

2130

++

++

1.18

—

—

n

19

—

102.2
101.4

7.4

5.3

—

—

80

3100

3330

++

++

1.95

0.227

54

tt

20

—

100.8
99.2

Fast-day

—

—

3300

2420

+++

+++

2.02

0.256

—

tt

21

—

100.8
99.2

tt

—

—

3300

2225

+ +++

+++

2.16

—

—

tt

22

—

99.4
99.0

tt

—

—

3900

2780

+++

++

2.20

—

—

tt

23

—

99.0
97.0

tt

25

175

3525

3535

++

+

2.08

—

—

tt

24

■—

99.8
97.0

tt

35

245

3900

3520

+ +

+

1.49

3.260

57

tt

25

~

99.2
97.6

22.3

L5.9

—

30

447 >

5200

2232

+

+

3.80

"

—

416 CHAPTER ni

Weight and Nutrition— '^ tight at admission 39.4 kg., at discharge 36 kg.;
i.e., a loss of 3.4 kg. The lowest weight was 34 kg. on Mar. 20, following the
most extensive undernutrition. Some fluctuations in the weight curve were caused
by sUght edema. The diet prescribed at discharge represented nearly 1.4 gm.
protein and 42 calories per kg., reduced by the weekly fast-days to 1.2 gm. pro-
tein and 36 calories average. Notwithstanding the loss of weight there had been
improvement in strength and comfort, and the patient was now walking 3 miles
daily and otherwise exercising without weariness.

Subsequent History. — On June 19, the plasma sugar was 0.161 per cent, CO2
capacity 52 per cent. June 30, sugar 0.156 per cent in whole blood, 0.172 per cent
in plasma, CO2 capacity 63.6 per cent. The weight was still 36 kg. Strength
had greatly increased, and the only complaint was of hunger. The urine had
remained consistently normal. The diet was increased to 60 gm. protein and
1550 calories. Glycosuria remained absent until Nov., and the general condi-
tion was excellent. Readmission was necessary Dec. 8, 1916, because glycosuria
was then persistent.

Second Admission. — Weight 37.2 kg., without perceptible edema. General
condition good. Acidosis was shown only by the heavy ferric chloride re-
actions and the ammonia nitrogen of 1 gm. Instead of immediate fasting,
Dr. Joslin's plan of a low fat-free diet was used. Thus, the diet on Dec. 9 con-
sisted of lean meat and green vegetables, representing 40 gm. protein, 20 gm.
carbohydrate, 10 gm. fat, and 336 calories. With gradual diminution of this diet
to 20 gm. carbohydrate and 9 gm. protein on Dec. 16, the ferric chloride reaction
became negative, the ammonia fell to 0.74 gm. N, and glycosuria diminished to
traces. It is noteworthy also that the total nitrogen excretion at first was 13
gm. daily. This progressively diminished on the semifasting to the low figures
of 4.71 gm. on Dec. 14, 4.76 gm. on Dec. 15, and 4.37 gm. on Dec. 16. A single
fast-day on Dec. 17 cleared up the lingering traces of sugar. To protect body pro-
tein, 40 gm. protein daily were immediately given, without carbohydrate, and
with fat so strictly limited that the total calories amounted to only 600. The
patient was dismissed temporarily on this diet on Dec. 22, 1916, to be home for
the Christmas holidays. Weight 34.4 kg.; strength and spirits good.

Third Admission. — Jan. 8, 1917. Patient returned according to arrangement, "■
saying that she had enjoyed the hohdays greatly. Weight 34.3 kg. Very slight
edema of legs. The diet remained at 40 gm. protein and 600 calories.

On Jan. 11, sore throat was complained of, but temperature was normal. On
Jan. 12, the temperature rose as high as 100.6°. On Jan. 13'; it was not above
100°. On Jan. 14, the weight was 32.2 kg., and the temperature up to 103.4°.
There were signs of typical pneumonia of right lower lobe; sputum showed Type
IV pneumococcus; blood culture negative.

The conditions during this attack of typical lobar pneumonia in a severely
diabetic patient are best shown in Table XVII. No alkali was employed.

Beginning Feb. 3, the protein was increased to 40 gm. daily. Thereafter the
total calories were gradually mcreased to 900. Beginning Feb. 10, the protein

CASE RECORDS

417

TABLE XVII.

Date.

1917
Jan. 13

" 14

" IS

" 16

" 17

" 18

" 19

" 20

" 21

" 22

". 23

" 24

" 25

kg.
32.6

32.2

32.3

32.1

31.7

31.8

94.4
100.0

102.0
103.4

104.2
103.5

103.822.3
101.6

104.022.3
102.0

102.8
100.6

102.2
101.4

100.8
99.2

100.8
99.2

99.4
99.0

99.0
97.0

99.8
97.0

99.2
97.6

Diet.

gm.

4.3

8.6
18.3

22.3

7.4

0.9

10.9

15.9

15.9

15.9

5.3

If

gm.
10

20

8.2

Fast-day.

22.3 15.9

25

35

30

Is

61

125

209

240

240

240

80

175

245

447

2100

3562

3800

3025

3700

3900

3100

3300

3300

3900

3525

3900

3200

Urine.

2547

3017

2265+

3238

2943

2130

3330

2420

2225

2780

3535

3520

2232

+

+

+

+

++

+ +

+ + +

+++ +

++ +

++

+ +

+

■a

+

+

++

++

+++

+++

++

+

+

0.80
0.57
0.70
0.83
1.260.227

0.268

1.18

1.95

2.02

2.16

2.20

2.08

1.49

+

0.80

Blood
plasma.

0.227

0.256

0.260

vol,
per
cent

68

60

54

57

418

CHAPTER m

TABLE XVII — Continued.

J3

1

H

Diet.

1

Urine.

Blood
plasma.

Date.

1

i

A

II
o

1

1

i

i

12:

i

6
o

1917

ke.

°F.

gm.

gm.

gm.

gm.

cc.

cc.

gm.

per
cent

vol.
per
cent

Jan. 26

—

98.6
97.8

30.0

40.5

—

10

569

3250

2526

+

0

0.88

"

~

" 27

—

98.6
97.6

30.0

40.5

—

5

534

3550

3016

+

0

0.86

0.118

—

" 28

—

98.4
97.4

30.0

40.2

—

20

637

3672

2913

+

0

0.72

—

—

" 29

—

98.8
98.2

30.0

40.2

—

7

532

3405

2758

+

0

0.84

—

—

" 30

—

98.6
97.0

30.0

40.6

—

10

60S

3415

3278

0

0

0.68

—

—

" 31

—

98.6
96,8

30.0

40.6

—

20

640

3470

3043

0

0

0.57

—

—

was raised to 50 gm., and Feb. 17 to 60 gm., and the total calories were gradu-
ally raised to 1300. Also 15 gm. carbohydrate daily were introduced with no
glycosuria or ketonuria at any time. The ammonia nitrogen was 0.48 to 0.68
gm. The blood sugar was 0.12 per cent, the lowest yet attained in this patient.
The plasma bicarbonate was 66 per cent. The patient was discharged on this
diet Mar. 9, 1917, weighing 31 kg. The diet thus represented nearly 2 gm. pro-
tein and 42 calories per kg., diminished by weekly fast-days to an average of 1.7
gm. protein and 36 calories per kg. Absolutely, the diet was low. In view of
the emaciation and the attendant lowered metabolism, it was relatively liberal.

Subsequent History. — The condition was excellent up to Apr. 11, then glycosuria
began to recur and the patient lost control of it. She was readmitted May 23
on this account.

Fourth Admission. — Weight 32 kg. There was heavy glycosuria, with only
fault traces of ferric chloride reaction. Blood sugar 0.326 per cent, CO2 capacity
63.4 per cent. Fasting was begun immediately, with 300 cc. coflEee, 300 cc. soup,
and 3 gm. salt daily. The ferric chloride reaction immediately disappeared.
Glycosuria fell to traces within 24 hours, and was negative in less than 48 hours.
Nevertheless, fasting was continued imtil May 27, when a tolerance test with

CASE RECORDS 419

green vegetables was begun, with 10 gm. carbohydrate and increasing 10 gm.
daily, as usual. Glycosuria appeared only with 60 gm. carbohydrate, June 1 and
2. The tolerance of SO gm. would thus indicate an increased assimilation to the
extent of 20 gm. as compared with the earlier test in Mar., 1916. A mixed diet
was then built up, until a trace of glycosuria appeared on June 7 with 60 gm. pro-
tein, IS gm. carbohydrate, and' 1300 calories. The ration was then fixed at 46
gm. protein, 10 gm. carbohydrate, and 1100 calories, and the patient discharged
on this in good condition, June IS, 1917, weighing 31.1 kg. The diet thus repre-
sented almost 1.5 gm. protein and about 35 calories per kg., diminished by weekly
fast-days to 1.3 gm. protein and 30 calories average. The CO2 capacity of the
plasma remained between 62.5 and 66.8 per cent throughout, the ammonia nitro-
gen between 0.37 and 0.77 gm. The blood sugar gave the only unfavorable indica-
tion, for with sugar-free urine it was found as high as 0.220 per cent and never
below 0.166 per cent.

Subsequent History. — The patient has remained in good condition, free from
symptoms.

Remarks. — The diabetes seemed to run a less rapid course in this patient than
in most of her age, but without radical measures the end must have been fairly
close when she was first received. The opportunity for restoring anything ap-
proximating normal condition was past, ,and the tolerance had been brought per-
manently and irretrievably low. The patient has been kept alive IJ years since
then, at a sacrifice of 8 kg. weight. It is to be emphasized that except for occa-
sional periods of greatest rigor, she has been stronger and more comfortable and
has actually looked better, according to her friends' judgment, than at the higher
weight. She remains continually cheerful, fairly well satisfied, faithful to the diet,
and strong enough for light labor and amusements, spending much of her time
outdoors and evidently taking pleasure in Mfe.

The usual recrudescence of diabetic symptoms with infection, and the smooth
and uneventful recovery of a severely diabetic patient from typical lobar pneu-
monia on the undernutrition which was requisite to ward ofi acidosis, are also
features of interest.

On the other hand, the gain of 20 gm. carbohydrate tolerance is too little
return for the loss of 8 kg. weight. If by any means the weight could be built
up by several kg., the tolerance would undoubtedly be less than at the first ad-
mission, and according to this standard there has been downward progress.
Such progress is fully accounted for by the general policy of feeding too close to
the limit of tolerance and thus keeping up slight overstrain of the assimilative
function as shown by the persistent hyperglycemia. If in Apr. and May, 1916,
the low blood sugar had been kept continuously normal, by fixing the body
weight at 33 or 34 kg. and the diet at its present figure of about 1100 calories, with
inclusion of a little carbohydrate, it is believed that the condition would today
be more favorable as respects weight, strength, and laboratory findings. It is the
old story of refraining from bringing the patient down to the necessary level of
undernutrition for therapeutic benefit, and later being forced to accept a still lower

420 CHAPTER ni

level of nutrition by reason of the downward progress resulting from the over-
strain. The progress has been so slow even with the overstrain that it is hard to
see how any "spontaneous" factor can be assumed. Notwithstanding the pro-
longed periods of comfortable existence and freedom from symptoms, it is prob-
able that the slow aggravation will contmue to ultimate death from coma or
inanition unless the patient is radically taken in hand and undernourished far
more rigorously than would have been necessary at the first admission. It is
even doubtful if such an attempt can now atone for the lost opportunities of the
past, or if the assimilative function may not have fallen too low to support life
permanently at any feasible level of nutrition.

CASE NO. 63.

Male, age 13 yrs. Polish American; schoolboy. Admitted Feb. 22, 1916.

Family History. — Father and one brother are well. Mother dead, cause vin-
known. No diabetes or other heritable disease known in family.

Past History. — Measles, chicken-pox, scarlet fever. Otherwise healthy life.
No sore throats or other minor infections. No abnormalities of diet. Never
nervous or obese. Apparently a thoroughly healthy, active boy.

Present Illness. — Polydipsia and polyuria with loss of weight and strength began
1 year ago. He has spent most of the year in hospitals. On one occasion he
had to be taken to a hospital because he "became sleepy" after eating a large
quantity of cakes. About 6 weeks ago he was in an institution where he was
given bread and other starches and made to take long walks "to buUd him up."
He realized that the treatment was making him worse, and having heard of the
Institute came here of his own accord on Feb. 21. The CO2 capacity of the
plasma was then 37.2 per cent, but dyspnea and other clinical symptoms were
absent, so the patient was told to return in 3 days, when there would be room for
him. On Feb. 21, he ate | pound of pork, half a loaf of gluten bread, some fat,
and some cofiee and soup. That evening he is said to have appeared a little tired
and cold. At 4 o'clock the next morning he woke up with extreme dyspnea. A
physician pronounced him dying, and the father considered treatment scarcely
worth attempting, and it was due to the patient's own request that he was brought
to the hospital.

Physical Examination. — ^Height 142.4 cm. A well developed, moderately emaci-
ated boy with intense air-hvmger. Skin dry, cold, very white, and lips grayish-
blue. He is nevertheless intelligent when roused. Tongue red, dry, brown-
coated. Teeth and tonsils normal. No superficial glandular enlargement. Pulse
rapid and thready. Abdomen much distended, but not rigid or tender. Knee
jerks present but sluggish. Wassermann negative. Examination otherwise
negative.

Treatment. — ^Death seemed imminent durmg the ambulance trip, and stunulants
were used. On arrival at hospital the rectal temperature was too low to register
on the ordmary cUnical thermometer. Pulse 92; respiration 31, air-hunger type.

CASE RECORDS 421

The CO2 capacity of 12.3 per cent was the lowest witnessed in this series of cases.
Sodium bicarbonate was immediately begun in 5 gm. doses by mouth, and hot
water and soup were also given as freely as possible. The patient was surroimded
with hot-water bottles, and rectal tube, turpentine stupes, and enemas were used
to reduce meteorism. After 4 hours the rectal temperature was 94.2°, pulse 96,
respiration 34. There was a gradual steady rise thereafter, until by 7 o'clock the
next morning the temperature was 101°, the pulse 100, the respiration 44. Up to
this time (12 hours) 45 gm. sodium bicarbonate and 4200 cc. fluids had been taken
and 2180 cc. acid vurine passed, with the usual intense ferric chloride reaction
and 3.6 gm. ammonia nitrogen. By this time (Feb. 23) the CO2 capacity of the
plasma had risen to 26.8 per cent. Additional clinical details are shown in
Table XVni.

The parallel slowing of pulse and respiration with relief of acidosis is note-
worthy; also the strikingly rapid loss of weight, notwithstanding fluid, salt, and
alkali intake during the period of highest acidosis (Feb. 22 to 26).

On Mar. 2, when after 9 days of fasting the urine had been sugar-free for more
than 24 hours, feeding was begun with 10 gm. carbohydrate in green vegetables.
A trace of glycosuria immediately returned, but increased very little as the car-
bohydrate was raised to 35 gm. on Mar. 9. Meanwhile the ferric chloride re-
action had become negative. After a fast-day on Mar. 11, another test showed
a higher carbohydrate tolerance, glycosuria appearing only with 100 gm. carbo-
hydrate on Mar. 23. After a fast-day on Mar. 26, mixed diet was begun, in-
creasing up to 50 gm. protein, 15 gm. carbohydrate, and 1200 calories on Mar.
31 to Apr. 1, without glycosuria. Glycosuria appeared on the same caloric
intake with 50 gm. protein and 20 to 30 gm. carbohydrate the following week.
Also in the next week a diminution of protein to 40 gm. and carbohydrate to 5
gm., with increase of fat to make 1500 total calories, brought glycosuria on Apr. 15.
In the following week with the same protein, without carbohydrate, glycosuria was
absent with 1200 calories, but appeared when the fat was increased to make 1400
calories; it then continued with diminution to 1200 calories. As usual with the
effects of fat, the h5rperglycemia and glycosuria were stubborn, not ceasing with
the fast-day on Apr. 23, a trace of glycosuria recurring on Apr. 24, and the sugar
being still 0.232 per cent in whole blood and 0.250 per cent in plasma on Apr. 27.
Nevertheless, the condition was conquered by restriction of fat. With the same
40 gm. protein, Apr. 27 to May 4, glycosuria remained absent with caloric intake
up to 1000. An increase of protein to 60 gm. and of calories to 1200 brought a
trace of glycosuria on May 6. By this time the general condition was good and
considerable exercise was being taken. Perhaps on this accoimt the diet of 40
gm. protein and 1200 calories, which caused glycosuria up to May 21, was subse-
quently tolerated; and in Jime the increase to SO gm. and 1300 calories and fi-
nally Qune 29 to 30) to 70 gm. protein and 1500 calories brought no glycosuria.
In July the protein was diminished to 52 gm. and the calories to 1200, in order to
permit the introduction of carbohydrate. This proved successful, so that by
Aug., 30 gm. carbohydrate were tolerated with this diet. The course in hos-

422

CHAPTER in

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CASE RECORDS 423

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424 CHAPTER ni

pital was uneventful, except that dental examination revealed three carious
teeth, which were removed without ill effects. The patient was discharged
Aug. 3.

Acidosis. — The acutely threatening condition at admission was described above.
This patient was apparently the nearest to death of any of those who recovered in
this series. Also there appeared to be a real acute need for alkaU, and in this
instance sodium bicarbonate seemed to be hfe-saving. It seems improbable that
simple fasting and fluid would have proved sufficient to combat such an acute
deficiency of alkah and high acid production. Thereafter the plasma bicarbonate
ran a fully normal course without the aid of alkah, the ferric chloride reaction
rapidly diminished with fasting and became negative after Mar. 6, probably more
by reason of the continuous imdemutrition than the small quantities of carbo-
hydrate then given. It reappeared, as may be so often observed, on subsequent
occasions about the same time with traces of glycosuria, even though the quanti-
ties of sugar lost were trivial and there were no significant differences in diet as
compared with other times when the reaction was negative. The only evidence
of continued acidosis was the ammonia nitrogen of 0.85 gm. on July 1, but with
the aid of 20 to 30 gm. carbohydrate this had fallen to a normal level by the
end of July.

Blood Sugar. — With blood sugars of 0.35 and 0.4 per cent at admission, it is
conceivable that carbohydrate feeding would have been injurious from this
standpoint, and possibly would have increased the acidosis by aggravating the
diabetic condition. There was a fairly prompt fall in the blood sugar. The well
marked rise. Mar. 2 to 10, indicated the genuine intolerance for even the small
quantities of carbohydrate then allowed. The rapid change for the better with
continued imdemutrition was shown by the rapid fall to 0.123 per cent in whole
blood and 0.141 per cent in plasma on Mar. 15. Notwithstanding the increased
carbohydrate intake, the sugar on the morning of Mar. 21 was only 0.151 per cent
in blood and plasma. On the morning of Mar. 29, it had reached the nearly
normal level of 0.104 per cent in whole blood and 0.123 per cent in plasma.
Instead of maintaining this advantage, with the added benefits of mixed diet, the
fat intake was increased unduly, with the consequence of many traces of glyco-
suria and continuous hyperglycemia. With the improvement in tolerance the
curve tended shghtly downward, to 0.145 per cent in whole blood and 0.159 per
cent in plasma on July 15. Then the simple increase of carbohydrate without
change in total calories brought a further elevation to 0.179 per cent in whole
blood and 0.182 per cent in plasma on July 29. As samples were taken before
breakfast and hyperglycemia was presimiably greater during digestion, it is
evident that the renal threshold was high.

Weight and Nutrition.— Weight at entrance 27.8 kg., at discharge 25.4 kg.;
i.e., a loss of 2.4 kg. The strength rapidly returned, especially with the aid of
exercise, and except for thinness and a persistent pallor (the latter perhaps nat-
ural) the boy appeared and acted normal. The diet prescribed at discharge was •
52 gm. protein, 25 gm. carbohydrate, and 1200 calories, representing approxi-

CASE RECORDS 425

mately 2 gm. protein and 48 calories per kg., reduced by weekly fast-days to
1.7 gm. protein and 41 calories per kg. The diet was absolutely low in view of
the age and subnormal weight. The objection to it is that it was in excess of the
assimilative power as demonstrated by the blood sugar.

Subsequent History. — The patient began school in Sept., and was able to do
everything like other boys. He prepared, weighed, and cooked his own diet,
and remained free from glycosuria. On Sept. 11, sugar in blood and plasma was
0.278 per cent (after 2 meals), CO2 capacity 55.8 per cent; weight 27.4 kg. He
had to be readmitted Nov. 20, 1916, because of difficulty with glycosuria, which
began on catching cold and then became unmanageable.

Second Admission. — Weight 26 kg. SUght glycosuria, negative ferric chloride
reaction. Patient still strong and comfortable, and normal to physical examina-
tion. Because of the stubbornness of the sUght traces of glycosuria, a 4 day
fast was imposed, reducing the weight to 24.2 kg. A diet of 30 gm. protein and
320 calories then brought back traces of glycosuria. The ferric chloride reac-
tion remained negative; and the ammonia nitrogen, which was 1.2 gm. the first
day, diminished to 0.5 gm. On Nov. 24 to 25, a diet of 30 gm. protein and 320
calories brought back traces of glycosuria, requiring a single fast-day on Nov. 26.
This glycosuria was evidently due to the suddeimess of beginning diet; therefore
on Nov. 27, 7 gm. protein and 80 calories were permitted, with an increase of
about the same quantity daily, until a trace of glycosuria reappeared with 45
gm. protein and 480 calories on Dec. 2. Dec. 4 to 16, a diet of 40 gm. protein and
600 calories caused almost daily traces of glycosuria, notwithstanding the usual
weekly fast-days. These ceased on the simple withdrawal of 100 calories of fat
beginning Dec. 18, protein continuing at 40 gm. Thereafter it became possible
to increase the calories first to 600 and then to 700. Also, beginning Jan. 1,
2.5 gm. carbohydrate were introduced, and increased to 10 gm. by Jan. 4. The
only evidence of acidosis was found in the ammonia nitrogen of 0.97 to 0.48 gm.
This seemed to be perceptibly diminished by the carbohydrate, for after its
introduction the range was 0.58 to 0.29 gm. The patient was dismissed on Jan.
10, weighing 25.2 kg., still in good condition although not so strong as before.
The diet mentioned represented nearly 1.6 gm. protein and 28 calories per kg.,
diminished by weekly fast-days to 1.4 gm. protein and 24 calories average. This
period of 2 months in hospital therefore represented extreme undernutrition, the
aim being only to protect body nitrogen with as high a protein intake as per-
mitted by the limit of tolerance. It is imfortunate that nitrogen balances were
not carried out. During fasting, Nov. 21 to 23, the daily urinary nitrogen was
5.24, 4.74, and 4.41 gm. No analyses were made of the 450 cc. soup taken daily.
Numerous analyses at other times indicate that the possible nitrogen content of
this quantity might range from 0.6 to over 2.0 gm. Later, 4 widely separated
days during the period of 40 gm. protein intake showed figures in close agreement,
between 6.74 gm. and 7.48 gm. urinary nitrogen. With allowance for the above
mentioned nitrogen taken in soup, this probably indicated nitrogenous equilibriiun.

426 CHAPTER III

The body nitrogen was seemingly spared effectively, but no material was pro-
vided for growth. Also body fat must have been sacrificed continuously, and the
relatively small loss of weight must have been due in part to water retention
masking the actual loss of substance. The boy was discharged only temporarily
on account of homesickness, and was instructed to report in 2 weeks'.

Third Admission. — Nothing further was heard from the patient until he was
readmitted in incipient coma on Feb. 12. It might seem that diabetic coma is
not strictly a single or imiform condition, for at his first admission this boy
showed chiefly dyspnea and extremely low blood alkahnity, with intelligence
apparently as clear as the state of collapse permitted. This time the same boy,
with CO2 capacity of 26 per cent, showed moderate dyspnea and disproportionate
stupor. The treatment this time was conducted without alkaU. Owing to other
work the laboratory study for this period is incomplete. No blood examinations
were made, except the one at admission which showed CO2 capacity 26 per cent
and sugar 0.425 per cent. The case shows how treatment can be conducted essen-
tially on the basis of chnical sjrmptoms and qualitative reactions. The available
data are shown in Table XIX.

The diet was built up in Mar. to 35 gm. protein and 600 calories, which caused
occasional traces of glycosuria. Toward the close of Mar. this diet was tolerated,
and was later increased to 45 gm. protein and 850 calories. The attempt to in-
troduce 10 gm. carbohydrate in Apr. caused only temporary glycosuria, but was
given up after Apr. 28 in order to increase protein to 55 gm. The patient was
discharged May 5, 1917. Height 142.4 cm. Weight 25.9 kg. Diet 55 gm. pro-
tein and 750 calories (2.1 gm. protein and 29 calories per kg., diminished by the
weekly fast-days to 1.8 gm. protein and 25 calories per kg.). He was definitely
weaker and worse off than before, but even on this low diet was able to be about
and was cheerful and courageous.

Subseqiunt History. — The patient was seen on June 8, weighing 24.8 kg., and
feehng brighter and stronger than on leaving hospital. He had shown shght
glycosuria ui the first week at home, but thereafter had been sugar-free. He
spent his time about the house and garden, raismg vegetables and chickens,
weighing and cooking his own diet, and keeping a complete record of diet and
urine tests. The ferric chloride reaction was negative. Plasma sugar (during
digestion) 0.264 per cent, CO2 capacity 49.1 per cent.

• Fourth Admission. — ^July 20, a telephone message was received from one of the
family that the boy had broken diet by eating bread and fruit, that he had heavy
glycosuria and seemed sleepy. Upon bringmg him to the hospital, heavy sugar
and ferric chloride reactions were found in the urine, but there were no cUnical
symptoms of acidosis. Weight 23.6 kg. The urinary conditions cleared up very
easily and the boy was discharged Aug. 10, 1917, on the same diet as before.
Hyperglycemia was persistent as before.

Suhsequeni HMtory.— Another relapse occurred and the boy was taken to a public
hospital, where he died Oct. 11, 1917.

TABLE XIX.

Diet.

Date.

1917
Feb. 12

i

n

kg

24.8

13

14

15

16

17

18

19

20

21

22

23

24

25

23.8

22.6

23.1

23.0

22.

23.0

23.4

23.7

23.8

24.0

24.0

°P.

97.2

97.6

98.2
99.6

99.6
97.2

95.6
97.6

96.4
98.2

!97.4
98.1

97.4
99.4

96.2
98.0

96.4
97.6

96.4
97.6

96.4
96.0

96.4
98.0

24.0

24.0

96.0
98.0

95.8

76
84

86
68

76
70

46
70

60
40

80
50

48
76

50
98

68
52

54
70

44
60

76
50

68
50

64

97,8 40

20
20

20

24

24
20

60
16

16
16

16

22

17
20

18
18

18
16

18
20

16

18

16

18

20
15

16
16

gm.

0

gm, gm, gm.
Fasting; 200 cc. soup.

400 " coffee.

600 " soup.

400 " coffee.

600 " soup.

400 " coffee.

600 " soup.

400 " coffee.

600 " soup.

22.3

15.9

—

22.3

15.9

—

22.3

15.9

—

22.3

15.9

—

22.3

15.9

—

22.3

15.9

—

22.3

15.9

—

22.3

15.9

—

7.4

5.3

—

240

240

cc,
1502

5000

5000

2500

2500

2500

2500

Urine.

806

5090

3611

2388

1918

2366

2126

240

2500

240

2500

240

2500

240

2500

240

2500

240

2500

80

2500

++++

++++

+++

++

++

+++

++

++

2346 + +

2397

2468

2643

3413

2488

+

+

+

+ + + +

+■+ +

+

+

+

0

427

428 CHAPTER III

Remarks. — ^The case is characterized by continuous downward progress, for
which two causes are known. One is extreme youth. Though the boy did not
gain in weight, nor to any significant extent in height, yet the growth impulse or
general metabolic strain of youth may be held responsible for the unfortunate
prognosis for diabetes of this grade of severity at this age. Nevertheless, it must
be recognized that a defiiute improvement in the power of assimilating food is
demonstrated by the record of the first period in hospital, so that the power to
recuperate was not wholly lacking, even in this chUd. The second known factor
is the excessive diet, which brought back hyperglycemia after the blood sugar
had fallen to normal, and would have been responsible for downward progress
even in an adult imder the same conditions. The low diet was not used at first
by choice, and therefore had to be used later by compulsion, after the real oppor-
tunity had been lost. Irrespective of the ultimate prognosis in such a case, the
duration of life and comfort may vary as much as several years, according to the
eflSciency of treatment and the earliness with which it is begun. In this instance
the boy was ready to die after 1 year of indifferent treatment, which had brought
the tolerance almost to zero, and was thereafter kept alive a year and a half,
most of the time in greater strength and comfort than during the earlier period
under other treatment.

CASE NO. 64.

Male, age 12 yrs. American Jew; schoolboy. Admitted Feb. 24, 1916.

Family History. — Father, mother, and one sister are well. No diabetes or
other heritable disease known in family.

Past History. — Fully healthy life except for measles and mimips. No sore
throats, toothaches, or minor infections known. Appetite, digestion, bowels
normal. Never nervous or under strain; always ranking well in school, and pro-
ficient in outdoor sports.

On Dec. 1, 1915, he fell down a flight of 10 stairs, landing on the front of his
head. There was no cut in the skin, no imconsdousness, no bleeding from ear or
nose, no paralysis or any perceptible symptoms beyond the slight bruise. The
patient did not associate the accident at all with his present iUness.

Present Illness. — ^About 3 weeks before admission there was acute onset of poly-
dipsia and polyuria, but not polyphagia. There has since been very rapid loss of
weight. Patient nevertheless continued at school until 1 week before admission.
He then saw a physician, who diagnosed diabetes and prescribed only a moderate
reduction of carbohydrate. During the present week the boy became increas-
ingly sleepy, and has spent ahnost his entire time for several days past sleeping
on a couch.

Physical Examination.— Hei^t 142.5 cm. Normal development, moderate
emaciation. Patient sleepy but easily roused. Moderate dyspnea of air-hunger
type. Face is that of a mouth breather and suggests adenoids. Cheeks flushed.
Skin dry and cracked. Mouth and Ups dry; teeth poorly kept, several carious;
some pyorrhea. Tongue and pharynx red and dry; tonsils do not protrude, but

CASE RECORDS 429

show pus on pressure. Few small palpable lymph nodes in neck, axillae, and
groins. Knee jerks obtamable by reinforcement. Exammation otherwise nega-
tive. Later examination by a rhinologist showed nose and ears normal, no ade-
noids, tonsils moderate in size, yielding considerable creamy pus on pressure.

Treatment. — On the day of admission the bowels were moved with calomel and
magnesium sulfate. Fasting was begun immediately because of the imminent
coma, 300 cc. clear soup and 3 to 5 liters total fluid being given daily. Within
24 hours, the CO2 capacity of the plasma rose from 16.6 to 27.7 per cent. The
D:N ratio had apparently been high, for on the first fast-day it was 2.65: 1, and
on the second day 1.43 : 1. On the second fast-day (Feb. 25) 25 gm. sodium bicar-
bonate were given. It was unnecessary, since the progress was favorable without
it, but seemed to produce an effect quickly in making the patient brighter and less
drowsy. Thereafter no alkali was given. Both glycosuria and acidosis rapidly
diminished, and on Feb. 29, after more than 24 hours of sugar-freedom, 2.4 gm.
carbohydrate were given. Green vegetables were increased progressively and
it became necessary to add potatoes, green peas, and lima beans before the limit
of tolerance was reached with 330 gm. carbohydrate on April 2 to 3. Mixed diet
was then begun without difficulty, and the patient was soon taking 2 or 3 nule
walks and other exercise daily. Four decayed teeth were extracted unevent-
fully and the mouth brought into good condition. The tonsils were not re-
moved. The patient was discharged May 5, 1916, feeling and appearing per-
fectly well and strong.

Acidosis. — Even with the low CO2 capacity of 16.6 per cent, it was evident
that treatment coxdd have been easily and safely conducted without alkali. The
use of sodium bicarbonate on 1 day, however, seemed to hasten results. The
ammonia nitrogen of 1.88 gm. on the day of admission covered ISJ hours.
The ammonia on Feb. 25 (2.36 gm. N) showed little perceptible effect from the
bicarbonate. On Feb. 26, it was 2.42 gm., on Feb. 27, 2.34 gm.; and only then,
with the CO2 capacity almost normal and the ferric chloride reaction down to
traces, did the ammonia show a real fall. Seemingly it was the active neutraliz-
ing agent which permitted the spontaneous rise in blood alkalinity. Subse-
quently acidosis was entirely absent by all tests.

Blood Sugar. — The hyperglycemia of 0.25 per cent showed a prompt fall to
normal, characteristic of an early case even though severe in symptoms. The
thoroughly normal course of the blood sugar as estimated mornings before break-
fast is one of the striking features of this case.

Weight and Nutrition. — The weight at admission was 25.2 kg., at discharge
25.6 kg.; i.e., a gain of 0.4 kg. There was visible edema only with the sharp
rise of weight up to Mar. 5, as so often happens on vegetable diet after fasting.
It is to be supposed that there was loss of body substance during treatment, with
retention of water due especially to the carbohydrate supply"; in contrast to the
dried tissues at admission. The evidence lies in the fact that on Apr. 3 the
weight was 1.8 kg. more than at admission, though the fasting and vegetable
period for 5 weeks had represented prolonged undernutrition, especially in pro-

430

CHAPTER III

tein. After Apr. 3 there was presumably some rebuilding of tissue, but the
weight diminished by 1.4 kg. The diet at discharge was 65 gm. protein, 50 gm.
carbohydrate, and 1750 calories. It thus represented about 2.5 gm. protein and
64 calories per kg., reduced by weekly fast-days to 2.25 gm. protein and 55
calories average. The diet was thus abundant for growth. Such a caloric
burden would produce downward progress in almost any adult diabetic.

Subsequent ffis^oj-j).— Progress seemed favorable tmtil on Mar. 20, 1917, the
boy had to be readmitted because of the development of persistent glycosuria.

Second Admission— Utight 142.4 cm. Weight 28 kg. Appearance hke that
of a normal boy. The very slight ferric chloride reactions were deceptive, for the
true grade of the acidosis was shown by the high ammonia and low CO2. The
data for the early stage of treatment are shown in Table XX.

TABLE XX.

Diet.

1

a .
0 '^

i

Urine.

Plasma.

Date.

i

p2

ll

1

1750
1750
1757
910
834
766
766
462
307
307
307

1

H

s

3.1

1

1917

Mar. 21
" 22
" 23
" 24
" 25
" 26
" 27
" 28
" 29
" 30
" 31

Apr. 1

gm.

65.0
65.0
65.0
65.0
65.0
65.0
65.0
31.4
18.5
18.5
18.5

em.

137.6

137.6

138.3

47.3

39.1

31.7

31.7

13.9

2.9

2.9

2.9

Fast

gm.

50
50
50
50
SO
50
50
50
SO
SO
SO
day.

gm.

30
30
30

30

24

kg.

28.0

27.4
28.4
28.7
28.5
28.5
28.8
29.0
29.0
28.8
28.7
28.6

cc.

1460
1530
1980
1410
1828
1270
2032
2094
1885
1976
1855
840

++++

++++

++++

+++

+++

+++

+++

+++

+++

++

++

0

++
++
+
+
+
+
+
+
+
+
+
+

gm.

10.16
10.70
11.25
6.56
8.56
7.70
8.84
6.01
4.82
5.62
4.49
3.13

gm.

2.13
1,88
1.23
0.94
1.33
0.73
0.67
0.34
0.38
0.38
0.28
0.26

ml.
per cent

38
41
60

56

so

70
67

In this case it is seen that diminution first of fat and then of protein, without
changing carbohydrate, reduced glycosuria so that it was abolished by a single
fast-day instead of several. On the other hand the high ammonia, notwith-
standing the large alkaU dosage, indicates persistence of acidosis. There was no
such rapid clearing of acidosis as is usually seen with fasting.

Apr. 2, a test with green vegetables was begun, with daily addition of 10 gm.
carbohydrate in the usual manner. Faint glycosuria occurred with 100 gm. car-
bohydrate on Apr. 11. The test was not carried further to learn whether this
was the true limit, but it seems strongly probable that a marked fall in tolerance
had occurred since the previous admission. A mixed diet was then begun, of

CASE EECOSDS 431

60 gm. protein, 30 gm. carbohydrate, and 1000 calories, including 200 cc. milk.
The blood sugar before breakfast on Apr. 13 was 0.110 per cent. Carbohydrate
was gradually increased up to 55 gm. on Apr. 27, with no glycosuria. The patient
was discharged again in apparently excellent health on May 2, 1917. The pre-
scribed diet was 60 gm. protein, 50 gm. carbohydrate, and 1250 calories, repre-
senting, for the body weight of 26 kg., 2.3 gm. protein and 48 calories per kg.,
reduced by weekly fast-days to 2 gm. protein and 41 calories per kg.

Subseqiient History. — The patient spent his time reading and playing at home.
On Jime 2, 1917, he weighed 26.2 kg., but a trace of glycosuria was found. The
diet was diminished to 45 gm. protein, 25 gm. carbohydrate, and 1000 calories.
There was a suspicion that the trouble had been due to overstepping diet. On
June 27, he reported again, weighing 25.8 kg., with normal urine, blood sugar
0.138 per cent, CO2 capacity 55.2 per cent. The same condition has continued
since. The patient is contented on his diet, attends school regularly, and ex-
pects to graduate from grammar school this year. He behaves and appears like a
normal boy, except for being noticeably thin.

Remarks. — This was one of the most rapidly progressive cases of juvenile dia-
betes, coma being imminent within 3 weeks of the first known symptoms. In one
respect such symptoms are advantageous, in that they call prompt attention to the
condition and afford the opportunity for early treatment. As usual, a high car-
bohydrate tolerance was quickly recovered in this case. The blood sugar also
became normal as tested mornings before breakfast, though the existence of ab-
normal digestive hyperglycemia must be assumed. As usual, a luxus diet re-
sulted in downward progress. It then became necessary, as usual, to reduce the
diet even lower than would have been required for proper treatment in the first
place.

Measures may soon be taken to reduce the persisting hyperglycemia. Owing
to the mistreatment during the most hopeful stage, the patient can never appear
like a normal boy again, but with suitable care it may be possible to preserve
the present condition of fair strength and comfort for a long, perhaps indefinite
time.

CASE NO. 65.

Male, married, age 53 yrs. American; business man. Admitted Mar. 6,
1916.

Family History. — Father died in old age, with diabetes for some years pre-
viously, though it was not the direct cause of death. A brother died of Hodgkin's
disease. History otherwise negative.

Past History.— MesLsles in childhood. Diphtheria at 14. Two attacks of
"gravel" 14 and 16 years ago; no trouble since. 6 or 7 years ago began to notice
cramp-like pains in calves of legs after long walking. On the whole, he has been
a healthy, hard working, prosperous man of rather large business affairs, but
without special strain. Appetite good, but not excessive. Acid stomach com-
plained of for past 5 or 6 years. Slight constipation; little exercise. No special

432 CHAPTER in

indulgence in alcohol, tea, or coffee, but the smoking of 8 or 10 strong cigars
daily is a fixed habit. Sleep normal. No nervousness.

Present Illness. — Onset not known. In 1914, life insurance was obtained, with-
out abnormal urinary findings. Patient has continued to feel well and work
efSciently. No polyphagia, polydipsia, or polyiiria. Eyesight may have failed
to undue extent. Occasional headaches. Persistent cough for 3 months before
admission. No hemoptysis, fever, chills, or sweats. The one symptom noted has
been gradual loss of about 15 pounds weight. On this accoimt he consulted a
physician, who found blood pressure 170-150, a trace of albxmiiniuia, and 3
per cent glycosuria. The patient was badly frightened at the word diabetes.
His physician slightly restricted starches and referred him to the Institute.

Physical Examination. — ^A well developed, well nourished man, shghtly over
weight. Rales without consoUdation, especially in lower lobe, left limg. Blood
pressure 160 systoUc, 80 diastolic. Examination otherwise negative.

Treatment. — With only a trace of glycosuria, there was nevertheless hyper-
glycemia (fasting) of 0.212 per cent in whole blood and 0.244 per cent in plasma.
Acidosis was absent by aU signs. Glycosuria ceased quickly on a diet of 100
gm. protein, 50 to 75 gm. carbohydrate, and 1800 calories. A green vegetable
period was begun with 25 gm. carbohydrate on Mar. 12 and 50 gm. on March 13.
Glycosuria appeared only with 220 gm. carbohydrate on March 28 to 29. The
patient was placed upon a diet of 90 gm. protein, 75 gm. carbohydrate, and 2200
calories, on which he was discharged Apr. 6. The weight had been reduced by 1
kg. The blood sugar had been brought to normal by the imdemutrition of the
carbohydrate period (Mar. 25) and had subsequently risen, especially on mixed
diet, to 0.147 per cent in whole blood and 0.131 per cent in plasma. In view of
the age and the mildness of the case, the hyperglycemia could be trusted to take
care of itself if the patient followed diet and reduced his weight as instructed.

Remarks. — The question is often asked whether fasting is necessary for patients
who readily become sugar-free without it and whose diabetes is mild. The general
principle is undernutrition. This patient had no fast-days. A carbohydrate
period is an agreeable means of undernutrition, and is furthermore useful as af-
fording a standard of tolerance for comparison with some later time. By June
the patient's weight was down to 59 kg., and by Aug. to 58 kg. He now esti-
mates his diet instead of weighing it. There has been no return of symptoms.
It is probably more important for such a patient to weigh himself than his food.

CASE NO. 66.

Female, age 15 yrs. American; schoolgirl. Admitted Mar. 6, 1916.

Family History. — Healthy, except that a paternal grandfather had diabetes at
time of death.

Past History. — ^Adenoids and tonsils removed in infancy. No illnesses, except
measles 4 years ago. Life and habits normal. Not neurotic. No excessive
appetite or indulgence in sweets. Menstruation began at 12 years, was regular
and normal up to Dec, 1915, when it stopped.

CASE RECORDS 433

Present Illness. — 5 months ago (Oct., 1915) patient had an attack of urticaria
from unknown cause. She was instructed to drink much water, and when unusual
thirst began thereafter she supposed it to be due to the habit of drinking. 1
month before admission she was seen by a physician, who did not examine the
urine and pronounced her in good health. On accoimt of the continuance of
excessive thirst she was taken to another physician 1 week ago, who made the
diagnosis from the lurine.

Physical Examination. — Height 158.1 cm. A well developed and normally
nourished girl with healthy color and no visible abnormahty. Blood pressure 90
systolic, 60 diastolic. Examination normal throughout.

Treatment. — The patient had been on practically unrestricted diet except for
abstinence from sugar. With the heavy glycosuria there was a trace of ferric
chloride reaction. Instead of the usual fasting, limitation of the diet, especially
in fat, was employed. On Mar. 7 the diet contained 51 gm. protein, 45 gm.
carbohydrate, and only 17 gm. fat. Carbohydrate was then diminished while the
calories were kept at approximately 800. Mar. 14 and 15 were almost fast-days, the
latter being a green day with only 10 gm. carbohydrate. Glycosuria and keto-
nuria being absent, the usual test with green vegetables was instituted. Traces of
glycosuria appeared on Mar. 22 to 23 with 80 gm. carbohydrate, but did not indi-
cate the true limit of tolerance, which was only reached with 140 gm. carbohy-
drate on Mar. 29 to 30. Mixed diet was then begun, and allowances of 70 to 90
gm. protein, 25 to 65 gm. carbohydrate, and 1750 to 2200 calories were tolerated.
Instead of fast-days, the patient took each week a day of six eggs, 450 cc. soup,
and 60 gm. bran. Anemia was foimd to be present, with hemoglobin 75 per cent,
and no ceU changes to characterize the condition. Examination by rhinologist
showed ears and nose normal, but cheesy deposits in crypts of the tonsillar rem-
nants. The anemia was treated with fresh air, exercise, and iron. The only
special event while in hospital was an attack of supposed appendicitis at the end
of May. Without any other symptoms, a trace of glycosuria appeared on May
29 on a diet within the demonstrated former tolerance. It cleared up spontane-
ously, but on May 31 the patient woke up with abdominal pain and nausea with-
out vomiting. There was some rigidity, slight tenderness, polymorphonuclear leu-
kocytosis, and temperature of 99.8° and 100.8°. From the double standpoint of
appendicitis and diabetes very little food was given from May 31 to June 2. With
rest in bed the abdominal symptoms quickly subsided, and beginning June 3 the
diet was cautiously btiilt up to the former level. The patient was discharged
June 29, feeling and appearing entirely well and exercising freely though not
strenuously.

Acidosis. — Owing to the mixed diet, acidosis was absent at admission, aside
from the trace of ferric chloride reaction. The CO2 capacity was normal, and
the ammonia nitrogen only 0.52 gm. Although, as stated, the diet on Mar. 7
was as nearly fat-free as convenient, the simple limitation of carbohydrate was
followed by a moderate ferric chloride reaction, a rise of ammonia to 0.89 gm. N,
and a fall in CO2 capacity from 56 to 48 per cent. On Mar. 8, with a diet of 59

434 CHAPTER m

gm. protein, 69 gm. carbohydrate, and 36 gm. fat, the ammonia rose to 1.6 gm. N,
and the COa fell to 44 per cent. Carbohydrate was then diminished ahnost to
Zero, keeping protein the same, while fat was gradually increased to S3 gm. On
this arrangement the ferric chloride reaction became negative, the ammonia fell
to 0.85 gm. N, and the CO2 capacity rose to normal without the use of alkali.
The explanation of this effect of diminished carbohydrate and increased fat Ijes
in the undernutrition, which amounted to a partial fast. Also the relief of the
overtaxed metabolism, by stopping glycosuria, tends to stop acidosis, even though
accomplished by dimim'shing carbohydrate. It must be added that this last sen-
tence does not contradict the first in this paragraph. The tendency to acidosis
accompanying diabetes can for some time be overcome by sufficient carbohydrate
in the diet.

With the abdominal attack on June 2, a trace of ferric chloride reaction ap-
peared. This and the slight irregularities in the CO2 curve may have been due
entirely to greatly reduced diet.

Blood Sugar. — The high percentage of 0.61 per cent in whole blood and 0.73S
per cent in plasma at admission were merely the accompaniments of an acute case
on carbohydrate-rich diet. With the simple restriction of diet stated, there was
an abrupt faU within 24 hours to 0.277 per cent in whole blood and 0.294 per cent
in plasma. Thereafter, with a more gradual decline, a fuUy normal value was
reached on Mar. 16. Subsequently the fasting blood sugar was always found
normal.

.■ Weight and Nutrition. — Weight at admission 50 kg., at discharge 45 kg. The
diet at discharge was 80 gm. protein, 40 gm. carbohydrate, and 1900 calories
and included milk and a little bread. Three eggs were allowed on weekly fast-days.
The diet thus represented about 1.8 gm. protein and 42 calories per kg., dimim'shed
by the partial fast-days to 1.6 gm. protein and 36 calories average. With the
moderate exercise prescribed, this may be considered a fairly low diet for a girl
of 15, though not so low as advisable under the circumstances.

Subsequent History. — The patient was next seen on Nov. 8 and reports of nor-
mal urine confirmed. The blood sugar was 0.110 per cent; total acetone in the
blood less than 10 mg. per 100 cc. 2 kg. weight had been gained. The appearance
was that of perfect health.

i Second Admission. — Dec. 6 to 10 the patient was in the hospital solely for
observation. The fasting blood sugar on 3 days was 0.13 per cent. Otherwise
everything was normal, except for persistence of slight anemia. The diet was
reduced to 1500 calories, with 80 gm. protein and 45 gm. carbohydrate.

Third Admission.— Apr. 4, 1917. The patient suddenly developed heavy gly-
cosuria and was immediately brought to the hospital. On the regular prescribed
diet the glycosuria immediately disappeared, and had apparently been due to
error in diet. The weight was 50 kg., the fasting blood sugar 0.10 per cent.
After 4 days of observation on this diet a test with green vegetables was begun,
and only a trace of glycosuria appeared with 145 gm. carbohydrate on Apr. 18.
The test was not continued to learn whether this was the actual limit of tol-

CASE RECORDS 435

erance. It was demonstrated that the tolerance was at least as high as 1 year
previously. The blood sugar on the morning of Apr. 19 was 0.1 per cent, the
CO2 capacity 74 per cent. The 1500 calory diet was continued, keeping the pro-
tein at 80 gm. and raising carbohydrate to 60 gm. by substitution for a little fat.
Six eggs were allowed on fast-days. The weight at discharge on May 2 was 48.2
kg. The diet thus represented 1.66 gm. protein and 31 calories per kg., dimin-
ished by the partial fast-days to 1.55 gm. protein and 28 calories per kg.

Subsequent History. — On moving to the country for the summer the patient was
allowed to substitute thick coimtry cream for the poorer city cream, and when the
mother reported traces of glycosuria the carbohydrate was diminished from 60
to 45 gm. The reports of marked increase of weight then aroused suspicion, and
notwithstanding the record of vigorous health and continuous absence of glyco-
suria, the patient was ordered to return immediately to the hospital, where
these facts were ascertained.

Fourth Admission. — Sept. 10, 1917. Weight 55.4 kg.; a gain of 7.2 kg. since
last discharge, and 5.4 kg. more than at the first admission. The plasma sugar
on the afternoon of Sept. 10 was 0.159 per cent; and though glycosuria was ab-
sent, a heavy reaction developed as soon as the regular diet with 60 gm. carbo-
hydrate was given. The ferric chloride reaction was negative, but there was a
strong nitroprusside reaction. A 2 day fast was necessary to aboUsh the glyco-
suria, and the acetone reaction became still heavier. A carbohydrate test was
then carried out in the usual manner, and glycosuria appeared with 140 gm. car-
bohydrate. The tolerance was thus approximately the same as before. If any-
thing there was improvement, because the weight was so much higher at the time
of this test. The patient was discharged on Oct. 4 to resume her vacation in the
country.

Acidosis. — The plasma bicarbonate was continuously at a high normal level
(67.2 to 78.6 per cent) without the use of alkaU. Though the ferric chloride test
was always negative, the nitroprusside reaction was strongly positive all through
the carbohydrate test and also on the diet at discharge. In other words, as
much as 140 gm. carbohydrate without other food failed to abolish acetonuria
at this time.

Blood Sugar. — ^This was not only dangerously high in consequence of the over-
nutrition at admission, but was also stubborn, being 0.156 per cent on the first
fast-day (Sept. 12) and 0.154 per cent on the second fast-day (Sept. 13). On
Sept. 14, it was found to have fallen abruptly to 0.09 per cent. The subsequent
values were normal when taken fasting. A sample taken after eating lunch on
Oct. 2 showed plasma sugar of 0.123 per cent; i.e., distinctly higher than a normal
person would show after the same kind of a meal.

Weight and Nutrition. — The undernutrition in hospital brought the weight
down to 52.7 kg. For the purpose of further reducing weight, an undernutrition
diet was prescribed at discharge, representing 80 gm. protein, 50 gm. carbohy-
drate, and 1100 calories.

436 CHAPTER III

Subsequent History. — The patient continued to feel well and the urine re-
mained negative for sugar. Nitroprusside reaction was negative after Oct. 18.
She was slightly hungry on this diet. She returned by request for a brief obser-
vation in hospital.

Fifth Admission. — Oct. 23, 1917. Weight 51.7 kg. Blood and urine normal
in all respects. The blood sugar before breakfast on Oct. 26 was 0.098 per cent.
At various periods of digestion, Oct. 23 to 25, it ranged from 0.109 per cent to
0.119 per cent. The patient was discharged on the 3rd day (Oct. 26) oh a diet
of 70 gm. protein, 60 gm. carbohydrate, and 1275 calories, the plan being to
reduce weight somewhat further while giving a balanced ration and protecting
body protein.

Subsequent History. — The patient remains weU and is pronounced by her
mother the strongest and most energetic member of the family.

Remarks. — The diet prescribed at the first discharge was somewhat too high.
The functional overstrain was detected from the slight hyperglycemia, and the
diet accordingly reduced in fat and calories. The carbohydrate was actually
increased by 5 gm. With this well advised change, normal blood sugar was again
restored and the entire condition remained favorable. After the third admission,
a more dangerous situation developed from the neglect regarding the fat intake,
and this danger was masked by the reduction of carbohydrate. Serious damage
would certainly have resulted had not suspicion been aroused by the increase in
weight while the patient was seemingly in splendid condition. It is thus proved
by two experiences that the appearance of "spontaneous downward progress" can
quickly be produced in this patient by ovemutrition. With rational regulation
of the total diet, the subjective and objective appearance of perfect health has
been maintained to date with no sign of downward progress. The only danger
in sight at present lies in the patient's tendency to overstep her diet, particu-
larly by taking fat. Though the ultimate outcome cannot be predicted, it is
believed that if the mistakes committed in other cases are avoided, and early
and ef&cient treatment be employed, the progress in the great majority of cases
of juvenile diabetes can be at least as favorable as in this one.

CASE NO. 67.

Male, married, age 46 yrs. Spanish; lumber merchant. Admitted Apr. 20,
1916.

Family History.— A maternal aunt died of diabetes. A cousin on the father's
side had diabetes. No other heritable disease known in family.

Past History. — Healthy life with considerable business strain, but also consid-
erable recreation and outdoor exercise. No illnesses remembered except mild
childhood infections. Luetic infection at age of 18 with secondary eruption.
Has been treated with short courses of mercury for many years, but never con-
tinuously or with salvarsan. Tendency to nervousness and insomnia. Consid-
erable but not excessive indulgence in brandy, wme, beer, and cigarettes. The
appetite has also been rather large. Normal weight 85 kg.

CASE RECORDS 437

Present Illness.—In Dec, 1913, patient consulted a physician for a sensation
of heat Uke fever. Polyuria and other usual diabetic symptoms were absent.
The temperature was found normal, and 4.1 per cent sugar was found in the
lurine. Patient states that he lived on " broths" for 15 days and glycosuria ceased,
but a "blood test" still revealed diabetes. He soon afterward disregarded
diet, and after 3 months, thirst and loss of weight were noticed and the glycosuria
was found to be 7 per cent. Since then he has received treatment at a number
of watering places and under specialists on the European continent and in England.
In Spain he once underwent the Guelpa treatment with benefit. Glycosuria has
become more persistent with time, and acidosis, as evidenced by both ketonuria
and lowering of the alveolar CO2, has been present at least since 1914. He has
gradually lost 30 kg. weight.

Physical Examination. — A fairly developed, moderately emaciated man, with
intellectual and rather nervous face. Teeth poorly kept, marked pyorrhea.
Tonsils normal. No lymph node enlargement except a few palpable glands in
groins. Arteries not perceptibly sclerotic. Knee jerks absent. Repeated Was-
sermann reactions strongly positive.

Treatment. — Fasting was begun immediately, and carbohydrate was used as
liberally as possible with the idea of clearing up acidosis promptly. Notwith-
standing the mild clinical character of the diabetes, the tolerance in a carbohydrate
test was not above 150 gm. carbohydrate in the form of vegetables. Mixed diet
was then begun and increased rapidly to 110 gm. protein, 30 gm. carbohydrate,
and 2000 calorifes. A few sUght sugar and ferric chloride reactions recurred, but
on the whole this diet was apparently well tolerated, and the patient was greatly
improved subjectively. He was discharged on the above diet on Jiuie 16, 1916.

Acidosis. — The slightly subnormal blood bicarbonate quickly rose, and the
ammonia correspondingly fell to normal.

Blood Sugar. — This was 0.27 per cent on admission, but fell to normal with the
rapidity characteristic of an early or mild case. The later values were normal or
on the upper limit.

Weight and Nutrition. — Weight at admission 54.2 kg., at discharge 55.7 kg.;
i.e., a gain of 1.5 kg. Part of this was evidently water retention, for there was
no appreciable loss of weight during more than a month of fasting and under-
nutrition at the outset. The diet at discharge represented almost 2 gm. protein
and 36 calories per kg., reduced by the weekly fast-days to 1.7 gm. protein and
31 calories average.

Syphilis. — The diet was purposely raised to the verge of tolerance, partly be-
cause of the mildness of the case, but chiefly with a view to testing the effect of
syphilitic treatment. In hospital the patient received SO mercury inunctions,
each consisting of half a Parke Davis "mercurette." He was also given 4 in-
travenous doses of O.S gm. salvarsan. There were no reactions to the first
treatments, slight reactions to the later ones. After discharge, he was treated
with 50 more merciury inimctions of the same kind and 4 more salvarsan injec-
tions, which continued to cause slight reactions. The former -f 4- -H Wassermann

438 CHAPTER III

in the blood had become negative by Sept. 2. After return to Spain the patient
received treatment with neosalvarsan.

Subsequent History. — The patient went immediately upon discharge to a
nearby summer resort and adhered to the weighed diet. Glycosuria remained
absent. On July 12, sugar in whole blood was 0.145 per cent, in plasma 0.154
per cent; on Aug. IS, 0.132 per cent in whole blood, 0.151 per cent in plasma. The
patient complained slightly of chronic himger and weakness. An increase of
diet to 40 gm. carbohydrate and 2500 calories on July 25 resulted in slight traces
of glycosuria. A reduction was therefore made to 35 gm. carbohydrate and
2250 calories. The weight tended to fall; i.e., on July 12, 55 kg.; on July 25,
54.8 kg. In Oct. the patient returned to Spam, having a rough voyage and
showing glycosuria several times because of starch in the diet on shipboard. He
has tried to continue diet, but has not been successful in remaining sugar-free,
chiefly because of too high caloric intake, including alcohol.

Remarks. — Though syphihs is a possible etiologic factor in this case, it re-
sponded to dietetic treatment in the usual manner of a case of this type, whereas
antiluetic treatment, sufficiently thorough to render the Wassermann negative,
showed no appreciable influence upon the tolerance.

CASE NO. 68.

Male, age 23 mos. American Jew. Admitted June 13, 1916.

Family History. — Parents and one older brother living and well. A maternal
great grandmother and grandmother died of "old age diabetes" developing at
about the age of 75.

Past History. — ^A normal baby with never any iUness except an occasional slight
cold. Was entirely well when examined by a physician 3 months ago at time of
vaccination. Weight 1 month ago 25 povmds.

Present Illness. — ^About 1 month ago the baby was noticed to be not quite so
well, and hunger, thirst, and urine were increased. The diet had consisted of
cereals, vegetables, milk, cream, butter, and occasionally eggs. During this
month he has gradually lost about 5 poimds, but seemed bright and playful and
not iU enough to cause worry. 4 days ago (June 9) it was noticed that the breath-
ing was abnormally deep. Thereafter he became fretful, imwell, and somnolent.'
The respiration by today became alarmingly deep and rapid, and a physician
diagnosed impending diabetic coma.

Physical Examination. — ^Height 86.4 cm. A normal child, still fairly well
nourished. Cheeks flushed. Marked air-himger. Mind clear. Tonsils enlarged,
but not acutely inflamed. A very few shot-like glands in neck and axillae. Re-
flexes normal. Wassermann negative. Examination otherwise negative. '

Treatment. — The child was admitted at 9:30 p.m., showing intense glycosxuia
and ketonuria, a trace of albimiin, and numerous casts. The data of the initial
period are shown in Table XXI.

CASE EECOEDS

'439

The child was restless and irritalilfi ..and refused to take liquid. jq£ any Kind.
The bowels were moved by enema. _. Food or liquids being violently resista^, soup
and water were given by stomach, tulie during the day, along with sodmnk (Siloride
and bicarbonate. The bicarbonate seemed to act rather promptly in ditnSi^ning
dyspnea." On the morning of Jime 14, the breathing and general cond^tionljhad
not changed appredably. By Jxme'15, the tondition seemed only slightly beiiter.
Probably Owing to thirst created by 'the salt, the child occasionally dra,idr"mter
voliiatarUy,; -but was still mostly treated by gavage. Albumin and casts dlfeap-
peared.'On" June 16,^ the condition was better, but food and drink" were jktiU
refused. On June 17, liquids were still given by tube, but the patient begaip to
ask for food. On June'W,"lDO gm: thrice cooked asparagus^were given." On June
20, vegetables representing 10 gm. carbohydrate brought a return of glycosuria.
On June"21, a"diet Of~eggs7;teavy cresm, thrice boiled vegetables,"and' «
beguUj but thetolerance was so low that 20 grn. protein caused glycosuria,
of about 300 calories were cbntinued, with occasional fast-days, and the as^mi
lation gradually improved,-- -The-patient -was discharged on Oct. i^-th; paijints
having carefully learned the;method of diet. ■'' |

"^<;SfoiMl--'WKile it Ts possible ffiaf simple fasting with fluids and'"silt wbuld
have -averted the threatened coma, the small iioses of alkah seemed to be ystih:tly
ibenmcial. iEven with the alkali the blood -bicarbonate was rather slow in ris iS.
The child- subsequently reniamed-fTee-f-r-eJB,;aeidosisr-- F-romrSept-lS-t-b Oct. %
the total acetone inrthe blqod plasma varied between 5'and'9'mg;-^er 100 cc.U

Bteod Sugar.— Ti^~c^iTtsKows Me normilT^^^
An abnormaL-degree.' of .digestive hyperglyeemia. is npjL.exduded, |

Weight aM Nutrition. — Weight at admission 8.5 kg., at discharge 8.1 kg.
the firsf2 months the diet- was approximately IS to- 20 gm. protein- iand
. |calortes^aily, about 2 gm. protein and 40 calories per kg. The t6leran()e gri
iaily;rose, so, that at the end, 42 gm. "protein, 22.5 gm. carbo!hydrate7 and
iGaloHes-Gould-be-given,-(including loo. cc. milk) jraih-the'blD.od. sugar, remaining
as above shown. The diet j prescribed at discharge was 42| gm. protein, 15 •[
jcarbohydrate, and S'SO c'alones-CaboTir S-gm. protein andr^S^calories -per4cg.->7 I

Subsequent History. — The patient remained cheerful aiid well at home iand |f ree
'frbm'IgrycQsTinarrThe followml", bro;od: record was-ottained: On Oct-.--20- -Ijlpod
jsiigar 0.125 per centj'plasiha' bicarbonate 60.7 per cent; on Nov. 20, '-blood siigar
0.I2S;pefxent7plpmrslIgar0.t3:3-perT:enr.-- This fasting^^ a

jWarning of the begiiming--oi trouble- from: tfie excessive diet, which was ignoted.
INevertheless tHe'clinical condition coHtttmed apparently-favorable -mrtilan-atikck
of jgfippe at" Christmas. -:With thislie had'cou^h, feve#, 4ii^ heavy -glycosulria.
Ttepaifems7prtiaI!y"contfpfled-fhe:gl5'rosuria^
hastened to return the child .to the hospital. '■ :'.'■>

~5ecoMr^awmm;=^Jaiirl7-^^ kg.- The ferric chloride-reac-

jtion'Vas negative. "The ^cosuria' was s%ht, and ceased promptly on are-
jduced diet ofr 15 gm.iprotein^^and 160 calories, without fasting. Thiftwas rapidly
increased, and after an uneventful stay in hospital,1he patient was dismissed on

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442 CHAPTER ni

Jan. 24, 1917, weighing 8.1 kg., on a diet of 35 gm. protein, 10 gm. carbohydrate,
and 415 calories (4.3 gm. protein and 51 calories per kg., reduced by weekly fast-
days to 3.7 gm. protein and 44 calories average). For extraneous reasons no blood
analyses were performed.

Subsequent History. — The patient remained free from glycosuria except for
occasional slight traces, for which minor changes in diet were advised. The
weight on July 3 was still 8.1 kg. The diet was increased with a little bacon, and
glycosuria gradually developed. It did not cease on withdrawal of the bacon,
and the parents hesitated to employ fasting. One feature in the case was the
nervous strain which the prolonged invahdism of the child imposed upon the
mother. The course adopted therefore was to allow glycosxiria to continue on a
carbohydrate-free diet of 320 calories. The glycosuria remained moderate.
There was no serious acidosis, and the child was comfortaHe 'except for the pro-
gressive weakness. Death must occur before long.!"; It js noteworthy that the
tendency to acidosis seems to be no greater than in an adult.

Remarks. — The attempt to force a diabetic child to grow and develop on high
diet failed as usual. As the diet at first prescribed included milk and carbohydrate,
and was adequate in calories and liberal in protein, the possibihty of a specific
inability of a diabetic child to grow and develop properly is suggested.. Com-
parison of such a child with a normal chUd on an identical diet would be an

interesting and valuable experiment.

A diet as excessive as this, woiild quickly. bring disaster in any adult patient
with severe diabetes. It is only surprising that the baby was able to withstand
the injury so long. The record of blood sugars in -hospital illustrates- the fact
that absence of fasting hyperglycemia is not proof that the diet given is suita;ble.
Irrespective of any laboratory findings, downward progress cbutd'be eq)ected" with
certainty from such a strain upon a weakened metabolism. As usual^ithe^diet
which is not restricted at the outset from choice, is later restricted from neces-
sity. The child does not grow or thrive, and the only -result «f excessive-feed-
ing is the permanent injury produced. Whether downward progress is inevit-
able in an infant (as it probably often may be) or not, there Ts little doubt
that it can be delayed and both life and comfort longer maintained with a more
rational hmitation of food. J ' ~. '~~~~'. ; J

The failure to make the limitation, even on the appearance of warning hyper-
glycemia, long before the onset of glycosiuria, is anottefseHous' fault In the man-
agement, which either caused or hastened disaster. It leaves the question of
inevitable downward progress of infantile (Habetes undecided, and" merely proves
that such a patient does not possess any remarkable recuperative power on
account of his years. ~ ] ~ ~7

1" Coma death occurred early in Dec, 1917.

CASE EECOEDS 443

CASE NO. 69. '

Female, married, age 39 yrs. German Jew; housewife. Admitted Aug. 23,
1916.

Family History. — Father died of Bright's disease at 69. Mother died of cancer
of liver at 79. Patient has had five brothers and two sisters. Three brothers
are well; one has right-sided hemiplegia; one died of "creeping paralysis" at 49.
Both her sisters died in infancy of unknown cause. No known diabetes, gout,
obesity, tuberculosis, syphilis, or cancer elsewhere in family.

Past History. — A few ordinary childhood diseases. The only other illnesses
were two attacks of "vaginal cellulitis" in 1912 and 1914. The local swelling was
such that catheterization was necessary. The inguinal glands were tender and
there was temperature as high as 104.5° F. She has had a healthy hfe, always in or
near New York, but has been overwrought and neurotic and has tended to become
obese. She was married 14 years ago and has been separated from husband
for the past 4 years. She has been vmder strain as a housewife, directing a large
estabhshment. Menstruation normal, except for some hemorrhages in recent
years, said to be due to fibroids. No children; five miscarriages, all self -induced.
Venereal denied. No tobacco. Only a little wine occasionally. Food taken
very sparingly for a number of years in order to check the tendency to obesity.
Bowels regular until onset of diabetes.

Present Illness. — On Dec. 28, 1915, there was a distinct acute onset of marked
polyphagia, polydipsia, and polyuria. 2 weeks later, because of these and rapid
loss of weight and strength, a physician was consulted, who immediately diag-
nosed diabetes and referred her to an experienced internist. She spent most of
Feb. in a hospital under his care, and by fasting and very low diet became sugar-
free 5 days before leaving hospital. A nurse was with her for 10 days after dis-
charge, and freedom from glycosuria continued diuring'this time. Glycosuria
returned soon after the nurse discontinued supervision. Since then on several
occasions doctors are said to have given her up because of threatening coma. There
has been a tormenting pruritus vulvae. Much of her hair has fallen out. There
has been loss of weight as follows: Sept., 1915, weight 138 pounds; Dec, 129
pounds; Jime, 1916, 89 pounds; Aug., 1916, 82.5 pounds; i.e., a total loss of 55.5
pounds.

Physical Examination. — An emaciated, neurotic looking woman with sallow,
dry skin and anemic appearance, but no acute symptoms. She claims to be so
weak that she can scarcely move a limb, but tests show that she is not quite so
feeble. Eyes, mouth, and throat negative aside from pallor of mucous mem-
branes. Liver edge palpable 2 cm. below costal margin. Blood pressure 70
systolic, 50 diastohc. General lymph gland enlargement. Slight edema of legs
withvpittjing about ankles. Knee and Achilles jerks normal. Wassermann
reaction negative.

Treat^^nt.—The Ratient fasted Aug. 25 to Sept. 1 inclusive. In the subsequent
test with green vegetables, 10 to 20 gm. carbohydrate were tolerated on Sept. 2

444 CHAPTER III

and 3, but glycosuria appeared with 30 gm. on Sept. 4. Corresponding to this
low tolerance, it was necessary to employ very low carbohydrate-free diets there-
after. Apart from the severity of the diabetes, the greatest difficulty in hospital
resulted from her excessively neurotic nature. She was subject to fits of crying or
screaming and other irresponsible conduct, and though the condition improved
somewhat with relief from the diabetic symptoms, it was never satisfactory.
She was discharged on Nov. 27 with a view to continuing imdernutrition treatment
under her private physician.

Acidosis. — The highest ammonia nitrogen excretion was 1.81 gm., the lowest
plasma bicarbonate 42.7 per cent. This acidosis cleared up imder fasting without
alkali. Thereafter the CO2 capacity remained fully normal and the ammonia
output was only slightly elevated.

Blood Sugar. — The hyperglycemia of 0.344 per cent on the morning of Aug. 25
remained imchanged 24 hours later, then gradually diminished to 0.178 per cent
on the morning of Sept. 4. Thereafter, even on the extremely low diet employed,
it remained persistently high, the value of 0.156 per cent in the plasma in the last
analysis on Oct. 24 representing the lowest level observed. As usual with such
a degree of h3rperglycemia, traces of glycosuria readily occurred on any attempt
to increase the diet.

D:N Ratio.— Omitting the initial ratio of 4.5, evidently due to carbohydrate
of theformer diet, the ratios on the fast-days Aug. 25 to 28 were 2.12, 1 .85, 2. 12, 1.03.

Weight and Nutrition. — Weight at admission 37 kg., at discharge 35.7 kg.
Extreme undernutrition was necessary to control the severe diabetes during
the entire period of 100 days in hospital. The total intake was 2864 gm. protein
and 48,317 calories, or an average of 28.6 gm. protein and 483 calories daily. The
urinary nitrogen record is not complete enough to permit calculating the nitrogen
balance. Some of the figures for daily nitrogen output are conspicuously low;
e.g., 2.72 gm. urinary nitrogen on Sept. 5, and 2.62 gm. on Sept. 13. Neverthe-
less, there must necessarily have been a negative nitrogen balance. Between
Oct. 5 and 28, an experiment was performed showing the production of both
glycosuria and acidosis by addition of fat to the diet, as described in Chapter VI.
The diet at discharge was only 50 gm. protein, 10 gm. carbohydrate, and 730
calories, i.e. 1.4 gm. protein and 20 calories per kg., diminished by weekly
fast-days to 1.2 gm. protein and 17 calories average. The treatment was there-
fore incomplete, since the patient had not been brought into equilibrium. Even
with the extreme undernutrition required, she showed slight increase rather than
decrease in strength, especially subjectively.

Subsequent History. — The patient continued treatment for a period not exactly
known, and then was subjected to various diets by other physicians. She died
Feb. 23, 1917, supposedly in coma.

Remarks. — The diabetes was of genuinely great severity, and the psychopathic
disposition largely precluded success. More might have been accomplished by
stiU more stringent undernutrition, to control the symptoms more completely
within a shorter time, but the ultimate result must have been failure without
greater reliability on the part of the patient.

CASE RECORDS 445

CASE NO. 70.

Male, married, age 34 yrs. American; physician. Admitted Sept. 3, 1916.

Family History. — Mother once had a tumor of face, which was removed by
operation, and did not return; riature not known. She died of cardiorenal dis-
ease. Father living and well, aged 74. Two brothers are well. One sister died
of diphtheria in infancy.

Past History. — Healthy life in good hygienic surroundings. Measles in child-
hood. No illnesses, operations, or injuries since. Venereal denied. No ex-
cesses in food, alcohol, or tobacco. Never nervous. Life easy and pleasant
without financial or other worries. Normal weight 60 kg.

Present Illness. — Began in Sept., 1914, with polydipsia and polyuria, but no
polyphagia. The onset was apparently sudden and glycosuria was immediately
found. For a year he was on almost carbohydrate-free diet under experienced
care, with the usual quantitative restriction also in protein; nevertheless glycosuria
was never absent at any time. He has since become discouraged and therefore
has occasionally broken diet with bread or cake. During the past year he has
lost about 8 kg. weight.

Physical Examination. — A tallj extremely emaciated young man. Skin very
dry. Hair thinning rapidly. Gums receding, though teeth are well kfept. Knee
jerks absent. Blood pressure 85 systolic, 65 diastohc. Examination otherwise
negative. Wassermann negative.

Treatment. — The severity of the case and the results of initial treatment are
shown in Table XXII.

In the subsequent period on green vegetables, traces of glycosuria appeared
when the intake reached 100 gm. carbohydrate. Mixed diet was then rather rap-
idly built up, and the patient was discharged on Oct. 16 feeling much improved
in strength and comfort.

Acidosis. — The rapid clearing of the rather threatening acidosis on fasting
without alkali is shown in the table. By Sept. 17, the plasma bicarbonate had
reached 61.4 per cent, and acidosis remained absent thereafter, the plasma bi-
carbonate at the last analysis on Oct. 13 being 70.6 per cent. Analyses for
acetone bodies in the plasma were made on 11 days at irregular intervals. The
highest finding was 39 mg. total acetone per 100 cc. plasma on Sept. 29. Dim-
inution followed, so that on Oct. 13 the total acetone was 11 mg. per 100 cc.
plasma. The ammonia excretion in the last analyses up to Oct. 11 was 0.51 to
0.88 gm. daily.

Blood Sugar.— Though glycosuria was kept absent, hyperglycemia was present
most of the tune. From 0.143 per cent in whole blood and plasma on Sept. 17,
the blood sugar rose during the carbohydrate test to 0.213 per cent in whole
blood and 0.217 per cent in plasma on Sept. 24. It then gradually fell to 0.111
per cent in whole blood and 0.135 per cent in plasma on Oct. 9 and 0.100 per cent
in whole blood and 0.135 per cent in plasma on Oct. IL This was with 10 gm.
carbohydrate in the diet. With increase to 20 gm. carbohydrate daily, the final

446

CHAPTER in

analysis on Oct. 13 showed 0.179 per cent sugar in whole blood and 0.189 per cent
in plasma. The allowance was therefore diminished to 10 gm.

Weight and Nutrition.— Weight at admission 42.2 kg., at discharge 40.3 kg.
Edema was present at certain times in hospital, raising the weight as high as
44.8 kg. ; this subsided on salt-free diet. There was the usual gain in strength and
comfort with imdemutrition and reduction of weight. The diet at discharge
consisted of 70 gm. protein, 10 gm. carbohydrate, and 1500 calories; i.e., 1.7
gm. protein and 37 calories per kg., diminished by weekly fast-days to 1.4 gm.
protein and 32 calories average.

Subsequent History. — The patient remained comfortable and resumed his former
work. Slight glycosuria developed on two or three occasions, but was immedi-

TABLE XXII.

Date.

1916

Sept

4

S

6

7

8

9

10

11

12

13

14

Diet.

3.9

7.9

gm.

127 10

127 10

127 10

Fast-day.

0.4
1.5

10
20

1495
1495
1495

60

127

kg.

41.8

41.6

42.2

42.4

42.0

41.1

41.0

40

40.6

40.0

40.8

Urine.

1990
1780
1800
1780
1810
3370
2445
2420
2340
3540
2150

42.8
31.2
33.3
16.2

5.8

+

+

0

0

0

0

4.82
5.20
4.78
6.86
4.12

1.41
1.76
0.93
1.11
1.04
1.32
0.58

M U

U 01

++++

+++
+++

++

+

+

+

0

Blood plasma.

per
cent

0.294
0.291
0.238

0.208
0.175

o
o

vol.
per cent

39.1
42.1
51.0

55.7
52.2

ately checked by a fast-day. There was a further sUght diminution in weight. On
Dec. 19, an apparently sUght attack of influenza began. He was still up and
attending to regular duties imtil Dec. 23, when severe cough developed, and fever
and weakness forced him to go to bed. The highest temperature was 100.5°. The
weakness increased, and on Jan. 1 the respiration was noticeably rapid, the pulse
rapid and weak; unconsciousness came on about 3 p.m., and death occurred on the
morniug of Jan. 2, 1917. The local physician who attended him attributed the
death to infection and not to diabetes, and no urine examinations were made
after Dec. 23.

Remarks. — It seems possible that the terminal condition was really diabetic
acidosis of the fasting type, since the patient was eating practically nothing on
the final days and the tendency to acidosis with even a slight infection is well

CASE RECORDS 447

known. If this were the case, there might have been a chance of preventing the
death by simple measures. The patient may have fallen a victim to a simple
influenza infection by reason of his somewhat weakened condition, but the de-
sirability of consultation with someone having experience with diabetes is indicated
in conditions of this sort.

CASE NO. 71.

Male, age 9 yrs. American. Admitted Oct. 30, 1916.

Family History. — ^No diabetic or other heritable disease.

Past History. — Normal and vigorous child, with no known infections or illness
of any kind.

Present Illness. — 2 years ago, mother began to notice poljfphagia and polyuria
with bed-wetting. He received early treatment from Dr. Joslin in Boston, and
subsequently came to New York. Under the treatment he was continuously well
and sugar-free, playing like a normal boy and going to parties, always taking his
own food with hun. About the 1st of Sept. he was detected in the practice of
going downstairs at night to take forbidden food from the pantry. Heavy gly-
cosuria thus came on, which was not controlled by his New York physician.
Progress was rapidly downward, and recently there has been marked and increas-
ing drowsiness.

Physical Examination. — ^A fairly developed, moderately emaciated boy, stupor-
ous but not unconscious, with deep rapid grunting respiration, 30 per minute.
Temperature 96° F, pulse 124. Mouth and throat normal. No lymph node
enlargements. Abdomen rounded with tympanites. Testicles undescended.
Knee and Achilles jerks absent. Examination otherwise negative.

Treatment. — The cUnical record can be summarized in Table XXIII.

The patient was admitted at 12:50 p.m., Oct. 30. He could still be roused,
but immediately went to sleep. The stomach was washed out to remove remains
of previous food, and 30 cc. castor oil, 5 gm. sodium bicarbonate, and 200 cc.
water were given through the tube. A high colon irrigation removed considerable
feces and relieved tympanites. The bowels subsequently moved several times as
the result of the castor oil. The temperature fell at first to 95.6°, but with appli-
cation of heat gradually rose to normal by midnight. Notwithstanding fasting
and 20 gm. sodimn bicarbonate, the CO2 capacity of the plasma on Oct. 31 was the
same as at admission, and the patient was in full coma. The same treatment of
fasting with liquids and bicarbonate by stomach tube was continued, and on
Nov. 1 the patient became able to imderstand what was said to him aind to drink
voluntarily. On the following days he was conscious but not fully rational, and
more or less hyperpnea persisted.

After 6 days of fasting, glycosuria was still present, sugar and ketones in the
blood were higher than before, and the strength was plainly becoming exhausted.
Accordingly, on Nov. 6, food was given to the extent of two eggs and 5 gm. carbo-
hydrate in green vegetables, and on Nov. 7 a slightly higher diet. Bed sores
began to develop at this time, and death from weakness threatened. Therefore

1

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449

450 CHAPTER in

on Nov. 7, 200 cc. blood were taken from the father into sodium citrate, and in-
fused into the patient. The only result was a temporary improvement of
strength. Unconsciousness gradually came on, and death occurred at 10 a.m.
Nov. 8 in coma.

Acidosis. — The tirine gave no adequate indication of the degree of acidosis.
On the other hand, acetone bodies accumulated in the blood to a remarkable
degree, as if the renal elimination were defective. This renal impermeability was
perhaps of decisive influence for the fatal result. Albuminuria and casts were
present, as usual in such a condition. Food, even though smaE in amount and
composed largely of protein and carbohydrate with Uttle fat, was followed by a
return of coma. Of course, it cannot be said positively that coma might not
have returned even with fasting.

There is no chemical explanation for the death. The blood bicarbonate on
Oct. 31, the child being in coma, was identical with that on Oct. 30, when coma
was still absent. It was comparatively high on the days when coma was partially
reUeved, but was also far above the ordinary danger level up to the last determi-
nation. On the other hand, the acetone bodies in the plasma on Oct. 31, with coma
present, showed only twice the concentration present on Oct. 30 before coma; but
they rose as coma subsided, so that on Nov. 4, with coma symptoms mostly
absent, the concentration was over twice that on Oct. 31; with coma present.
Diminution of the ketonemia then followed as the clinical condition became worse,
though the figures remained high to the end.

Lipemia. — The high Hpemia at the outset was one of the striking features. It
diminished imder fasting, and though later analyses were not performed, the
plasma in the closing days was clear.

Blood Sugar. — This also was very high in proportion to the glycosuria. Such
an apparent renal impermeability for sugar may perhaps be a disturbing influence
in the attempt to reckon dextrose-nitrogen ratios. Except for such impermea-
biUty, high and perhaps maximal ratios might have been found. Also, the child
might have been better off if he could have excreted both sugar and acids freely.
The relatively low blood sugar of Nov. 1 is remarkable in comparison with all the
other figures. Otherwise the blood sugar changed Kttle or even incraesed sUghtly
on fasting.

Body Weight. — There was not the precipitous fall in weight characteristic of
fasting coma and desiccation. On the other hand, bicarbonate did not cause
edema. The total loss of 2.1 kg. weight is adequately accounted for by the pro-
longed fasting and rather free purgation, without the assumption of any abnor-
mahty of the water balance.

Remarks. — The child went into complete coma before fasting had time to exert
much influence. He then came out of coma and apparently might have been
saved if the strength had held out.

The treatment has not been satisfactorily worked out for patients with either
dangerous weakness or extreme intensity of intoxication. With regard to alkali,
some would employ larger dosage, while Joslin suspects an injurious effect and

CASE RECORDS 451

would perhaps suggest that the great increase of acetone bodies in the blood repre-
sented such a harmful influence of the alkali. With regard to diet, there are the
possibilities of simple fasting, carbohydrate feeding, and protein feeding. Fasting
alone often fails in this extreme condition. Carbohydrate perhaps could not be
burned at all, and the possible hyperglycemia consequent upon any large dosage
of carbohydrate, with the blood sugar aheady 0.5 per cent and poor excretory
power, presents a serious question. Pure protein diet might maintain strength
and furnish ammonia to neutralize acids. At the same time it might aggravate
the diabetes and nulhfy the possible benefit derivable from fasting. Various
persons will hold various opinions, but the fact remains that while impending coma
of ordinary type is generally readily cleared up, the patients presenting this excep-
tionally severe condition generally die.

With regard to the cause of death, the evidence in this case excludes the sup-
position of simple acid intoxication or deficit of alkali. Some may seek the ex-
planation in the toxicity of certain substances of the acetone group. Others may
see the cause in possible precursors of acetone bodies in the tissues. The, expla-
nation is wholly undecided. It is possible that no one substance is responsible,
but that death results from a more general alteration of cellular metabolism and
protoplasm.

CASE NO. 72.

Female, age 12 yrs. American; schoolgirl. Admitted Nov. 16, 1916.

Family History. — Parents hving; mother rather sickly, cause unknown. One
brother died in infancy. Two brothers and one sister are well. No diabetes
or other hereditary diseases known.

Past History. — Measles, mumps, and possibly chicken-pox. No infections re-
cently. Normal development, health, and habits.

Present Illness. — Patient began to feel unwell about a year ago, and a physician
diagnosed diabetes. She has since been on starch-poor, fat-rich diet, and applied
at the Institute on account of progressive weakness especially during the last 2
months.

Physical Examination. — ^A well developed, fairly well nourished child; high
color in cheeks; sUght edema of eyeUds and ankles. Deep rapid respiration sug-
gesting air-htmger. Tongue red and dry. Teeth poorly kept, two decayed;
pyorrhea present. Enlarged lymph nodes on both sides of neck. Knee jerks
very feeble. Examination otherwise negative.

Treatment. — At admission temperature was 100.2°, pulse 120, respiration 24.
After the first 24 hours the temperature remained between 98 and 99, pulse about
80, respiration 18 to 20. The data of this period in hospital are shown in Table
XXIV. No alkaU was used.

The case was rather unusual-in its slowness in clearing up. The only special
incident in hospital was the uneventful removal of the two carious teeth. Com-
plete control of the diabetes was never achieved, as shown especially by the
persistent hyperglycemia. The patient was discharged Dec. 23, 1916, on a diet
of SO gm. protein, 10 gm. carbohydrate, and 600 calories.

452

CHAPTER ni

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CASE EECOEDS

453

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454 CHAPTER III

Subsequent History.— Tht patient felt fairly well, played about with her friends,
and led an approximately normal life. Sugar and ferric chloride reactions
gradually returned about Mar. Particularly on Mar. 9, it is suspected that
candy was obtained surreptitiously, and later in that day shortness of breath
and drowsiness developed. On the morning of Mar. 10, these had increased and
nausea had come on, which prevented eating, but water was stiU taken in large
quantities on account of thirst.

Second Admission. — 11 :20 p.m.. Mar. 10, 1917. Child pale, with flushed cheeks,
semiconscious and delirious, in tjrpical diabetic coma. Temperature 96.8°,
pulse 97, respiration 36. Otherwise appearance and examination as before.

In addition to the usual urinary reactions, it was found that the CO2 capacity
of the plasma was 14 per cent, and the total acetone of the plasma 54.5 mg. per
100 cc. The stomach was washed out, and 20 cc. castor oil and 5 gm. sodium bi-
carbonate were given through the tube. A saline enema had Httle result. Sodium
bicarbonate was continued in 5 gm. doses, so that 25 gm. had been taken by 6
a.m. The coma gradually became deeper. The temperature gradually rose to
100°, the pulse to 138, the respiration rate remained 36 to 38. Death occurred
at 6:50 a.m. A blood sample taken shortly before death showed plasma bicar-
bonate 17 per cent and total plasma acetone 97.8 mg. per 100 cc.

Remarks. — ^With diabetes of this severity only imperfectly controlled by treat-
ment, downward progress is inevitable. The case illustrates the necessity of
prolonged and thorough hospital treatment if any results worth while are to be
achieved in the severest diabetes, though it is possible that any dietetic method
would have been inadequate to save this patient.

In connection with the rapid premortal rise of acetone bodies in the blood, the
question may be raised whether this was due to the administration of alkaU, and
whether sodium bicarbonate was harmful in this case. Similar premortal increase
of circulating acetone has been observed in patients receiving no alkali.

CASE NO. 73.

Female, age 3 jrrs. American. Admitted Dec. 18, 1916.

Family History. — Negative except for glycosuria in a paternal grandfather.

Past History. — Entirely healthy life; no known infection. Habits normal.

Present Illness. — ^About 1 year ago, thirst and loss of weight attracted notice,
and the patient then received fasting treatment for 3 weeks in a hospital under
the best care (Dec, 1915). Glycosuria was abolished and the tolerance was high,
so that she was finally able to take 46 gm. protein, 24 gm. carbohydrate, and 1000
calories. Only occasional traces of glycosuria appeared on this diet at home
until Oct., 1916. Since then glycosuria has occurred every 3 or 4 days, despite
increasing strictness of diet. The diet before entry contained 25 gm. protein,
5 gm. carbohydrate, and 430 calories.

Physical Examination.'^— Titi^t 88.6 cm. A poorly developed, emaciated, pale
and pinched looking child, without acute symptoms. Mouth and throat normal.

CASE RECORDS 455

Abdomen slightly distended, but soft. No lymph node enlargements. Exami-
nation otherwise negative.

Treatment. — Glycosuria was very slight and the ferric chloride reaction negative.
The traces of sugar persisted, however, not only on 25 gm. protein and 420 calories
but even on 20 gm. protein and as little as 250 calories. In a tolerance test with
green vegetables, increasing by 5 gm. carbohydrate daily, glycosuria was absent
with 20 gm., but appeared with 25 gm. carbohydrate. With gradual undernu-
trition the food tolerance rose slightly, and the patient was disch^fged on Apr. 7,
1917, free from diabetic symptoms but not otherwise improved.

Acidosis. — By reason of the former treatment, this was never present. The
plasma bicarbonate was normal, and the ammonia nitrogen on carbohydrate-free
diet was about 0.084 to 0.42 gm. daily, with total nitrogen output of some 3 to
5gm.

Blood Sugar. — This was 0.245 per cent at admission, and was not appreciably
affected by treatment, even though freedom from glycosuria was achieved.

Weight and Nutrition. — Weight at admission 9.8 kg., at discharge 8.9 kg. With
gradual undernutrition the patient became able in Jan. to take a diet of 22 gm.
protein and 350 calories. It gradually became possible to increase this and also
to introduce carbohydrate, so that she was discharged on a prescribed diet of 28
gm. protein, 7.5 gm. carbohydrate, and 550 calories (3.2 gm. protein and 62
calories per kg., reduced by weekly fast-days to 2.7 gm. protein and 53 calories
average). The carbohydrate was in the form of milk, and no reckoning was made
of the 300 gm. thrice cooked vegetables. The child showed no injury from the
0.9 kjg. loss of weight whUe in hospital, but on the other hand was no stronger,
and remaitted pale and puny, fairly comfortable, yet with her mind fixed on her
diet, Uke a severely diabetic adult.

Subsequent History. — Only rare traces of glycosuria have occurred at home.
There has been no sign of downward progress; neither has there been improvement
in tolerance, or anything resembling normal development. The small patient
merely leads an existence of semi-invalidism. She has recently been readmitted,
and the blood sugar brought to normal by the method described in Chapter II.
It is of interest that this was possible in a case of such extreme severity, but the
ultimate result is still doubtful.

Remarks. — The case is one of the severest and most hopeless examples of juve-
nile diabetes. There has been no improvement in assimilation. The ability to
remain free from glycosuria on a higher diet than at admission has merely been
purchased at the price of the sUghtly reduced weight. With regard to the ques-
tion of "spontaneous downward progress" in children, it is instructive to note
what a great loss of tolerance took place within 10 months on high caloric diet,
while no downward progress has been perceptible in the past 10 months on low
diet, even though the diabetes in the latter period is at a much more severe stage
than before.

456 CHAPTER rn

CASE NO. 74.

Male, unmarried, age 23 yrs. American; plumber. Admitted Feb. 1, 1917.

Family History. — Mother died from an operation of unknown character.
Father and two brothers are well. No diabetes or other heritable disease known
in family.

Past History. — Thoroughly healthy hfe. Never ill to his knowledge, even
with childhood diseases. Appetite, diet, digestion, and bowels normal. No
alcohol; moderate tobacco. Never had a medical examination before.

Present Illness. — 1 year ago began weakness and excessive thirst. He con-
sulted a physician within a month but received only a very lax diet sUp. 7 months
age he was forced to give up work and has continued to grow weaker. He has
lost about 45 poimds in aU.

Physical Examination. — Height 173.8 cm. A rather poorly developed, emaci-
ated yoimg man. Skin dry and pale. Perceptibly but not seriously drowsy.
Mouth and throat normal. Knee jerks absent. Wassermaim reaction nega-
tive. General examination negative.

Treatment. — Fasting was begun immediately and continued Feb. 1 to 4 in
elusive. 10 and 20 gm. carbohydrate were tolerated on Feb. 5 and 6, but 30
gm. caused glycosuria on Feb. 7, which increased with 40 gm. on Feb. 8. There-
after the diet was rather rapidly buUt up, and on 60 gm. protein and 1100 calories
there was decided improvement in general condition. In another green vegetable
period beginning Mar. 19, 100 gm. carbohydrate were tolerated without glyco-
suria. The weight at this time was down to 40 kg. The improvement continued
on an increased diet of 65 gm. protein, 10 gm. carbohydrate, and 1450 calories.
The patient was discharged on Apr. 27, 1917, much improved, though stiU not
strong enough to return to his regular work.

Acidosis. — The plasma bicarbonate of 36 per cent at admission rose steadily
without the aid of alkali to 55 per cent on Feb. 3, 57 per cent on Feb. 5, and 73
per cent on Feb. 8. Thereafter it remained at a high normal level. Ammonia
determinations were not made at first, so the highest ammonia nitrogen observed
was that of 2 gm. on Feb. 5. The ferric chloride reaction of the urine was only
slight at admission, diminished to traces on the first fast-day, and thereafter was
negative. Nevertheless, the anunonia nitrogen remained stubbornly elevated,
frequently as high as 1.5 gm. daily, except for a fall as low as 0.45 gm. during
the second carbohydrate test. At discharge it was still 0.8 to 1.4 gm. daily.
The ammonia excretion was therefore the most delicate index of acidosis and at
the same time evidence of an unduly high fat ration.

Blood Sugar. — The sugar in the plasma was 0.377 per cent at admission, 0.290
per cent on the morning of the second fast-day, and thereafter gradually dimin-
ished to its lowest level of 0.137 per cent at the last analysis on Apr. 14. These
values obtained mornings before breakfast showed that the hyperglycemia was
inadequately controlled, though the tendency was in the right direction.

CASE RECORDS 457

Weight and Nutrition. — Weight at admission 43.6 kg. Lowest weight 40 kg.
The diet of 65 gm. protein, 10 gm. carbohydrate, and 1450 calories at discharge
thus represented 1.5 gm. protein and 33 calories per kg., diminished by the
weekly fast-days to 1.3 gm. protein and 28 calories average.

Subsequent History. — The patient contracted a cold with heavy cough 3 days
after leaving hospital. He adhered to his diet and remained free from glycosuria,
but cough and weakness increased. He returned to report on May 29, 1917, and
was immediately readmitted.

Second Admission. — The patient was more emaciated and much weaker than
before. Weight 38.6 kg. Sugar and ferric chloride reactions negative; COj
capacity of plasma 64 per cent. He was kept in hospital until June 13, and on
carbohydrate-free diet of 75 gm. protein and 1500 calories showed neither gly-
cosuria nor dangerous acidosis. The ammonia excretion was about 1 gm. daily.
The temperature during the first 4 days in hospital was 102 to 103° F., there-
after 101°. Cough persisted. Physical examinations revealed nothing in the
right lung beyond fine moist rales at the base. Over the left lung there was
dulness from the apex to the fourth rib in front, to the fifth interspace in the
axilla, and to the middle part of the infraspinous region behind, with bronchial
breathing and coarse and fine moist rales. X-ray plates and the finding of tubercle
bacilli confirmed the diagnosis. As such a patient could not be kept long, he
had to be mioved on June 13 to a public hospital, and died on July 3.

Remarks. — ^The susceptibility of diabetic patients to tuberculosis is well known,
and this patient's weakened condition doubtless impaired his resistance to the
disease. The slight or absent influence of the infection and fever in producing
glycosuria or acidosis is noteworthy. With tuberculosis of this grade and such
severity of diabetes, the prognosis was necessarily hopeless.

CASE NO. 75.

Male, vmmarried, age 33 yrs. Irish Canadian; teamster. Admitted Feb. 21,
1917.

Family History. — Father died at 65, cause imknown. Mother alive, aged 60.
Three brothers and two sisters are well. As far as known, a perfectly healthy
family of laboring class.

Past History. — Measles and mumps in childhood. Never ill since. Venereal
denied. Patient is slight in build, but tough and wiry. Has lived rough out-
door life with heavy work as a teamster in Hudson Bay district. Thus had a
very high caloric diet, but well balanced. He has taken 5 or 6 drinks of whisky
or beer daily.

Present Illness.— In June, 1914, patient noticed polydipsia and polyuria with-
out polyphagia. Principal trouble was that all his teeth loosened and fell out.
Smce then he has been most of the time under fasting treatment at the Victoria
General Hospital at Halifax. He has been kept alive for this time, but the normal
weight of 130 pounds has fallen to 89 pounds. He was referred to this Insti-

458 CHAPTER ni

tute because of the great severity of his case, making it almost impossible to
keep him sugar-free on any living diet.

Physical Examination.— Kei^t 162.4 cm. A short, slight, small-boned young
man, extremely emaciated, but still cheerful, alert, and with a look of strong
constitution and unlimited resisting power. He still shows indications of his
former weather beaten life and sinewy musculature. There is a peculiar icteric
tinge to the skin of the face and thorax, while conjunctiva are clear. Hair thin
and dry. Teeth missing. Throat normal. Blood pressure 110 systolic, 80
diastolic. Knee jerks not obtainable even with reinforcement. Examination
otherwise negative.

Treatment. — He made the trip from Halifax to New York in this condition unat-
tended, and had the misfortune to be detained for a week by the immigration
officials. As he could not during this time receive suitable treatment, it was ad-
vised that he be fed protein and carbohydrate with as little fat as possible. Con-
sequently, he finally arrived at the hospital with heavy glycosuria; but with no
acidosis beyond a trace of ferric chloride reaction. On an observation diet of SO
gm. protein, 10 gm. carbohydrate, and 600 calories, glycosuria remained heavy.
Fasting was therefore begun on Feb. 23. Glycosuria ceased in 3 days, but the
fast was continued for 5 days. The tolerance was evidently too low to make an
attempt at a carbohydrate test worth while. Accordingly, the first food (Feb.
28) consisted of two eggs, with coffee, soup, bran, and 300 gm. thrice boiled vege-
tables. This diet was increased until on Mar. 8 glycosuria appeared on 60 gm.
protein and 800 calories. The patient is still in the hospital, and the tolerance
has gradually improved under treatment, so that he has sometimes for brief
periods taken diets as high as 95 gm. protein and 32O0 calories (fat and alcohol)
with little or no glycosuria. The opportunity has been taken of shifting the
diet in various ways for experimental purposes. The data are partly given in
Chapter VI.

Acidosis. — This has remained absent, except as slight ketonuria has been
deliberately produced and abolished at times in the course of experiments.

Blood Sugar. — Hyperglycemia, though not excessive (0.2 to 0.3 per cent)
proved stubborn, as usual in such a case. It has been more marked when the
true tolerance was experimentally exceeded. Nevertheless, it has since been
shown that the plasma sugar even in this case can be brought fully to normal
(0.066 to 0.11 per cent). Whether it can be made to remain so and whether the
cHnical result wiE be beneficial is an important question.

Weight and Nutrition. — The weight at entrance was 37.6 kg. Under treatment,
it touched a minimum of 33.4 kg. on Mar. 20. It has since been possible to
increase the weight to 38.8 kg. with no more than faint glycosuria (Aug. 14, 1917),
but it will again be reduced therapeutically. There has been no perceptible
edema. The diet has varied widely for experimental reasons, but has never
included more than 20 gm. carbohydrate. The above mentioned high diets must
be understood as only brief and experimental, and clearly injurious if continued.
In general the diet is a low maintenance ration in proportion to the emaciated
condition.

CASE RECORDS 459

Remarks. — The absence of knee jerks is supposedly attributable to neuritis or
some other nervous disorder, for, in contrast to the rule with most emaciated
diabetics, the muscles are not relaxed in this patient. He has remaiued clmicaUy
the same as at admission, always cheerful and alert, always feeling a Uttle hungry
and sometimes decidedly so, and as active as the fuel value of his diet permits.
He is thus up and about all day long, occupied with reading or other recreation,
and able to go on walks and visits outside the hospital when desired. He can-
not Hve outside an institution, partly on account of lack of education. The
diabetes is in the extreme stage where true recovery of assimilation has never
been known to occur. But during 9 months in hospital there has been not the
slightest indication of "spontaneous downward progress."

CASE NO. 76.

Male, age 4 yrs. American. Admitted Mar. 9, 1917.

Family History. — ^A maternal grandaunt and cousin had diabetes at the
time of their deaths, aged 55 and 60 years respectively. The famUy history is
otherwise negative for heritable disease. Parents and three older brothers of
patient are well.

Past History. — ^Normal birth. Breast fed for 9 months; always perfectly
healthy, mild whooping-cough being the only disease ever suspected. He took
a prize as a most perfect baby a year or so before onset of diabetes.

Present Illness. — ^An earache occurred on Feb. 17, 1917. A physician found
the temperature 103° F. With simple warm applications the pain promptly
subsided, and the ear has been normal since. On Feb. 22 the boy, still appearing
and feeling entirely well, was target shooting with his father, and intense polyuria
was noticed, the father saying that the boy urinated every 15 minutes. He
was immediately taken to the family physician, who made no diagnosis, but the
father is convinced that the urine was tested only for albumin. In addition to
intense polydipsia and polyuria, rapid loss of flesh was noticed, though the
amount was not determined by weight. As the family physician continued to
make Ught of the trouble, the father insisted on taking the boy on Mar. 6 to a
New York pathologist, who found glycosuria of about 8 per cent and positive
acetone reactions, and gave a prognosis of only a few months of Ufe. The family
physician then prescribed an antidiabetic diet with some oatmeal, and 2 days
later the boy was brought to this hospital.

Physical Examination. — Height 106.6 cm. The child is an admirable physical
specimen, fully developed and still well nourished, handsome, but with a pale
waxen beauty and listless apathetic behavior which augur badly. Axillary and
epitrochlear glands palpable. Reflexes lively. Blood pressure 90 systolic, 70
diastolic. Wassermann reaction negative. Physical examination normal.

Treatment. — The urine at admission showed only sHght sugar and ferric chloride
reactions. Fasting was begun immediately. The sugar immediately fell too low
to titrate, and was absent after 24 hours. After 2 days of fasting a carbohydrate
tolerance test was begun. On Mar. 21, 82.5 gm. carbohydrate were taken with-

460 CHAPTER ni

out glycosuria, but 90 gm. on the next day resulted in glycosuria. A mixed
diet was then gradually bxiilt up, and the patient showed no more glycosuria
up to his discharge on May 8, 1917.

Acidosis. — This was limited to slight ferric chloride reactions, and ammonia
excretion of 1.16 gm. daily. There were no clinical symptoms or lowering of the
plasma bicarbonate. During the carbohydrate tolerance test the ammonia
output fell as low as 0.05 gm., and there was no further evidence of acidosis.

Blood Sugar. — The usual hyperglycemia was present at admission. In sub-
sequent treatment the blood sugar was made and kept normal throughout.

Weight and Nutrition. — ^Weight at admission 15 kg., at discharge 14.4 kg.;
i.e., undernutrition to the extent of 0.6 kg. altogether. The diet was gradually
built up to SO gm. protein, 65 gm. carbohydrate (25 gm. in milk, 30 gm. in bread,
the rest in vegetables), and 900 calories. This represented nearly 3.5 gm. pro-
tein and 63 calories per kg., diminished by the weekly fast-days to about 3 gm.
protein and 54 calories per kg. The child still appeared normal and well nour-
ished but remained somewhat depressed.

Subseqiient History. — The patient lived his regular normal life with the other
children at home, spending most of every day in lively outdoor exercise. With
this his strength and spirits improved while the luine tests, in four periods every
day, remained continuously negative for sugar. Perhaps on account of the
exercise the weight remained stationary. He seemed to be in favorable condition
and steadily improving, and was readmitted to hospital on Sept. 12, 1917, solely
for observation. One noteworthy feature of both earlier and later stages of the
history has been the occurrence of occasional digestive upsets from slight or
imknown causes. The question of pancreatitis is open.

Second Admission. — Height 107.5 cm. j i.e., a growth of 0.9 cm. since first
admission. Weight 14.7 kg.; i.e., a gain of 0.3 kg. since discharge. On his pre-
scribed diet the blood sugar was normal (0.067 to 0.099 per cent) in repeated tests,
both fasting and at different periods of digestion. A carbohydrate tolerance
test by the usual method resulted in a trace of glycosuria only with 250 gm.
carbohydrate. It is not fully certain that improvement to this degree had actu-
ally occurred, for it is possible that the 90 gm. taken in the former test may
not have represented the true limit of tolerance at that time. The patient was
discharged Oct. 16, 1917, weighing 14.4 kg. (the same as at the former discharge)
with both urine and blood normal in all respects. The prescribed diet was 55
gm. protein, 80 gm. carbohydrate, and 980 calories, representing 3.8 gm. pro-
tein and 68 calories per kg., diminished by weekly fast-days to about 3.3 gm. pro-
tein and 58 calories average. This diet is permitted with the idea of permitting
the boy to grow if possible. A close watch is being kept, and any appearance of
slight hyperglycemia will be the signal for a reduction of diet. The carbohydrate
has since been increased to 100 gm., and the child is growing steadily, the blood
sugar remaining normal.

Remarks. — The case was received at a favorably early stage, and the treatment
has been followed with the utmost fidelity. The result in this 4 year old patient
is favorable to date.

CHAPTER IV.
PANCREAS FEEDING.

Since so many factors, dietary, psychic, and others, influence the
glycosuria in most cases of diabetes, the only valid material for testing
the specific influence of any therapeutic agent must consist of cases in
which the food tolerance is accurately known under exact dietetic
management for considerable periods of time. The use of drugs and
other agencies credited with power to influence diabetes has never
been supported by reliable tests of this character. Since diabetes is
accepted as a deficiency of the internal secretion of the pancreas, and
since a few other internal secretory deficiencies can be more or less
compensated by administering preparations of the organ in question,
the attempt to supply the internal pancreatic secretion in this manner
has appealed to investigators since the time of von Mering and Min-
kowski. Such attempts have uniformly failed in both animals and
patients. It seemed worth while, if only for the sake of negative
results, to make a few tests with the administration of fresh pancreas
to patients whose assimilative power was accurately known. As pan-
creas preparations are toxic when admim'stered parenterally, the fresh
gland was given by feeding.

By reference to the graphic chart of patient No. 1 (Chapter III) it
will be seen that diets of 75 to 100 gm. carbohydrate and 40 to 60 gm.
protein had been tolerated in May and June without glycosuria, or
with only small quantities of glycosuria toward the close of June as the
calories were increased by addition of fat. Pancreas feeding was
tried for a week, following the fast-day of July 9. The diet was the
same as during the previous 2 months; viz., nothing but vegetables
with the addition of a little cream, butter, or bacon on certain days.
The calories were thus kept very low and the only protein, aside from
that of the green vegetables, was in the form of pancreas. This con-
sisted of 100 gm. pancreas on July 10, 150 gm. daily on July 11-12,
and 200 gm. daily on July 13-14. The pancreas was obtained fresh

461

462 CHAPTER IV

from the slaughter house each day, so that the first portions were
eaten only a few hours after kiUing, and that taken at supper was still
less than 12 hours old. The pancreas was kept on ice except during
the messenger's trip, and was served raw with vegetables in the form
of a salad. It can be seen from the graphic chart that glycosuria was
absent with 80 gm. carbohydrate on July 10 and with 117 gm. carbo-
hydrate on July 11. On July 12, with 143 gm. carbohydrate, there
was glycosuria of 9.59 gm.; on July 13 with 92 gm. carbohydrate a
glycosuria of 5.54 gm.; on July 14 with 83 gm. carbohydrate, a glyco-
suria of 7.39 gm. This record may be compared with that of the pre-
ceding 2 months. For example, on May 23, 140 gm. carbohydrate
had been taken without glycosuria, and the total calories on that day
were higher than on any day during the pancreas period. There was
also no subsequent improvement of tolerance, owing to the week of
pancreas feeding, because, beginning July 16, diets somewhat lower in
carbohydrate, but with the addition of considerable fat, soon brought
on continuous glycosuria.

Patient No. 4, a 12 year old boy, developed a liking for raw pancreas,
and the opportunity was taken to carry out several feeding tests.
One series is described in detail in his history (Chapter III), and the
conclusion was there drawn that the pancreas did not improve the
carbohydrate tolerance to the extent of a trivial quantity of sugar,
and did not improve the protein tolerance to the extent of one egg.
Another test was undertaken in August and September. It will be
seen in the graphic chart (Chapter III) that there was a gradual in-
crease of carbohydrate-free diet beginning August 26. This diet
consisted of eggs, steak, olive oil, butter, and whisky, with no vege-
tables or other food. It will be noted that sugar and ferric chloride
reactions remained negative until the diet reached 58 gm. protein and
1300 calories on August 30. Ferric chloride reactions then developed,
followed by glycosuria of 0.75 gm. on September 1. The glycosuria
and ketonuria were continuous on the following days, until checked by
the alcohol days of September 5 and 6. Beginning September 7 a
similar carbohydrate-free diet was resumed, which on Septeniber 8
and 9 amounted to 60 gm. protein and 1600-f calories. On Septem-
ber 10, 100 gm. pancreas were substituted for the former 100 gm.
beefsteak. This happened to be the day on which a glycosuria of

PANCREAS FEEDING 463

0.32 gm. appeared. The pancreas was continued in the same quantity
on the subsequent days, and it is seen that glycosuria was continuous.
Also the ferric chloride reactions were actually heavier than before,
due doubtless to the gradual impairment of tolerance. It was neces-
sary on September 16 to stop this diet, and then two alcohol days were
inadequate to clear up this glycosuria and ketonuria which had de-
veloped on pancreas feeding. B eginning September 18, very low diets,
generally below 500 calories daily, were employed, and the attempt
was made to compare successive days of pancreas and steak feeding.
The results were interfered with because during this time the patient
obtained small quantities of food surreptitiously. All that can be said
is that these tests, which continued up to September 27, showed no
perceptible advantage of the pancreas. What is certain is that even
on these very low diets the pancreas feeding did not avail to prevent
glycosuria from even a few grams of bird-seed eaten by stealth.

The possibiHty was also considered that some portion of the benefit
in the way of improved assimilative power from fasting might be due
to the digestive rest involved. For example, it might be supposed
that the internal secretory function of the pancreas is more or less in-
hibited during activity of the external secretory process, while per-
haps the nervous, secretory, or glandular condition during the resting
state of the acinar tissue might be most favorable for the internal
secretory function. Inasmuch as the special stimulus to the formation
of pancreatic juice is furnished by the hydrochloric acid of the stom-
ach, experimental or practical results might be hoped for by admin-
istering food in some way which would not call forth acid secretion in
the stomach. Since rectal or parenteral feeding did not appear
promising, a trial was made with a tube like an ordinary Einhorn
duodenal tube, but over one meter in length, so that food might be
deHvered through it to a point low enough in the intestine to avoid
regurgitation into the stomach if possible, yet high enough up to per-
mit favorable absorption. Patient No. 8 was chosen as a suitable
subject. The method of procedure consisted in his swallowing the
tube slowly in the morning; after 2 or 3 hours the tube was generally
found in proper position for the first feeding, and was retained until
bedtime. The patient was very Kttle inconvenienced by the presence
of the tube. The position of the tube was tested in various ways:

464

CHAPTER IV

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466 CHAPTER IV

by fluoroscopic examination for the oKve or injected bismuth paste;
by the character of the fluids aspirated; by the absence of the feeding
mixture from the stomach when the tube was withdrawn after the
last feeding; by the fact that air injected with the oUve in the stom-
ach was soon belched up, whereas with the olive in the intestine it
was before long passed by rectum; and, to some extent, by the sensa-
tions of the patient.

The mixture used for feeding consisted of an emulsion of eggs, olive
oil, and small quantities of sodium bicarbonate. On other days the
patient drank these same foods in the raw condition for comparison
with the results of tube feeding. Whisky was never given through
the tube but was always drunk in 10 cc. doses at intervals during the
day. This allowance of whisky could not impair the results, since
whisky used during fasting does not spoil the benefit of fasting. Some
details are supphed by Table I and in the graphic chart (Chapter
III).

It was evident that the feedings by tube did not cause glycosuria
to such an extent as lower diets taken by mouth, but weight was lost,
the patient was markedly weaker, the urinary nitrogen did not cor-
respond to the protein administered, and the feces though formed,
were unduly bulky, so that it seemed probable that the results were
due to poor absorption of the food given by tube. Accordingly, on
December 18 similar emulsions were given freshly mixed with pow-
dered commercial pancreatin. Acidosis was manifested not only by
the ammonia nitrogen above 1 gm. (notwithstanding the alkali dos-
age) but still more by weakness and malaise on the part of the patient.
Accordingly on December 19, oatmeal gruel representing 44 gm. carbo-
hydrate was added to the feeding mixture, with a view to testing both the
assimilation of carbohydrate administered by tube and the possibiUty of
any special virtues of oatmeal. Heavy glycosuria promptly resulted,
the ammonia excretion slightly increased, and a period of imdernutrition
was necessary to clear up the symptoms. On December 30-31 the
tube was retained by the patient both day and night for the purpose of
maximal feeding. Only two eggs were given on December 30 and none
on December 31 ; otherwise the feedings consisted of olive oil emulsified
with 5 gm. pancreatin and large quantities of extract of fresh pancreas.
Over 2 kilograms of pancreas were used for this purpose. The glands

PANCREAS FEEDING 467

from cattle were obtained within a few hours after slaughtering,
minced in a meat grinder, and then subjected to a pressure of 4000
pounds per square inch in a hydraulic press. The thick, almost pulpy
extract thus obtained was diluted slightly with water, and partly used
fresh. The soUd residue of the glands was incubated with water,
olive oil, and a trifle of sodium bicarbonate, and pressed again after
digestion. The emulsion of this material was also administered by
tube. Glycosuria and acidosis persisted, though apparently absorp-
tion of the material was poor. This large feeding caused only diarrhea
without benefit, and the experiment was therefore discontinued.

The experiments with feeding fresh pancreas confirm the accepted
view that it possesses no value in diabetic treatment As far as a con-
clusion is possible from the experiments with tube feeding, they indi-
cate that there is no benefit in this method. There is no evidence that
simple avoidance of the production of hydrochloric acid in the stom-
ach, or of stimulation of- the external secretion of the pancreas, has
any influence upon either glycosuria or acidosis in diabetes.

CHAPTER V.
EXERCISE.

The existing literature may be summarized as having led to con-
clusions as foUows: that in normal persons, moderate exercise slightly
elevates the blood sugar while severe exercise lowers it, but in either
case the sugar tolerance is increased; that in mild diabetes, exercise
may elevate the blood sugar even more than normally, but neverthe-
less the carbohydrate tolerance is raised; while in severe diabetes,
exercise can no longer improve tolerance and must be avoided be-
cause of exhaustion of the patient and dangerous increase of acidosis.
The onset of coma after slight or severe exertion has especially been
known and drea4ed.

The use of exercise in the present work was based upon experiments
on dogs, which were carried out with the necessary completeness and
controls, and will be published in detail in the near future. Though
circumstances prevented carr3dng out corresponding comprehensive
tests upon patients, nevertheless exercise has been employed for the
past 2 years as part of the treatment of diabetic cases, most of them
severe beyond the degree formerly considered to contraindicate
exercise. A few definite experiments were conducted at the outset,
and some empirical experience has been gained since. The observa-
tions may be grouped under the following four heads :

A. Immediate effect of exercise on blood sugar.

B. The effect upon carbohydrate tolerance and glycosuria.

C. Its use in various classes of patients.

D. The more permanent effects upon assimilation and the diabetic
condition.

A. Tta; Immediate Effect of Exercise on the Blood Sugar.

Observations on Patient No. 18.

This patient represented the early mild stage of potentially severe
diabetes. By reference to the graphic chart (Chapter HI), it will be
noted that the test with vegetables alone, ending August 4, showed a

46S

EXERCISE

469

tolerance above 350 gm. carbohydrate. On August 6, a mixed diet
was begun of 100 gm. protein, 100 gm. carbohydrate, and 2600
calories. Beginning August 10, carbohydrate was gradually sub-
stituted for fat until 170 gm. carbohydrate were taken, which caused
no glycosuria on August 12 but a trace on August 13. After the fast-
day of August 14, the increase of carbohydrate was continued up to

TABLE I.
Patient No. 18.

Blood.

Urine.

1

Date.

i

to

g

i

Corpuscle sugar.'

SIS

"

13
1

^5

lOlS

ter
cent

ter

cent

ter cent

per

cent

ter
cent

°F.

Aug. 19 (rest) 2:20 p.m.

0.256

0.213

0.286

—

—

+ +

++

8:00 p.m.

0.250

0.250

0.250
(calc. 0.244)

100

37.0

Aug. 20 (exercise) 10:00 a.m.

0.150

0.156

0.133

100

—

0

+

98.2

10:50 a.m.

0.100

0.105

0.093
(calc. 0.094)

108

42.8

100.6

2:20 p.m.

0.099

0.116

0.100
(calc. 0.075)

105

41.2

100.4

8:00 «

0.222

0.238

0.182
(calc. 0.197)

110

39.7

98.8

Aug. 21 (exercise) 10:00 a.m.

0.111

0.111

0.109
(calc. 0.111)

100

41.5

0

+

98.6

10:50 a.m.

0.098

0.080

0.115

105

44.8

99.9

(calc. 0.120)

* The top figues for corpuscle sugar in all the tables are those obtained by direct
analysis. The figures in parentheses are those calculated from the relations of
whole blood and plasma.

200 gm. on August 18. With this, slight glycosuria appeared, and
continued on August 19. Keeping the diet unchanged, the following
observations were made.

No breakfast was taken. The two meals were eaten at fixed hours,
12:45 to 1:20 p.m. and 5:30 to 6 p.m. daily. It will be noticed in
Table I that the diet with 200 gm. carbohydrate had produced a

470 CHAPTER V

marked hyperglycemia, in blood samples taken 1 hour after lunch and
2 hours after supper on August 19, the patient having been up and
dressed but otherwise as quiet as convenient up to this time. Under
the dietary conditions stated, the hyperglycemia could safely be ex-
pected to continue or probably to increase. On August 20, without
food, the boy exercised between 10 and 10:50 a.m. to the Umit of
strength, running up and down 80 flights of stairs and walking briskly
between times. He then rested and took food as stated. During the
hour after lunch (1 :20 to 2 : 20 p.m.) he performed the hardest exercise
of the day, and continued with only short rests until supper time, the
afternoon's work amounting to 160 flights of stairs and almost continu-
ous brisk walking between. No exercise was performed after supper.
On August 21, exercise was performed between 10 and 10:50 a.m.,
comprising 88 flights of stairs and walking as usual.

Each flight of stairs counted includes both ascent and descent. A
flight was composed of 24 steps, each 16 cm. high. The boy ran rapidly
up and down, and by walking between times avoided stopping for
rest. He was strong and active, and though considerably tired by the
exertions, was never exhausted and always felt able to do more.

It is evident from the table that violent exercise stopped the exist-
ing glycosuria and markedly lowered the blood sugar.

Ketonuria, as far as could be judged by the ferric chloride reaction,
diminished rather than increased. This reaction alone is obviously
not a safe index. The possible alterations in blood bicarbonate
were not studied; but if there was a lowering it was evidently soon
restored by rest, for a single determination at 8 p.m. on August 20
showed 63.6 per cent.

Exercise concentrated the blood, as indicated by the higher hemo-
globin (Fleischl-Miescher) and hematocrit readings. Sugar analyses
were performed directly upon the corpuscles, after 15 to 20 minutes
centrifugation at 3000 revolutions per minute. These furnish inter-
esting controls, but are subject to errors, on the one side from ad-
herent plasma, on the other side from possible imperfect laking of
the corpuscle mass in analysis; so that the calculated values are to
be preferred. No special effect of exercise is apparent upon the
distribution of sugar between plasma and corpuscles. If there was,
for example, any such thing as a longer retention of sugar in the

EXERCISE 471

corpuscles than in the plasma, equilibrium evidently was reached
within an hour, for analyses an hour or more apart failed to reveal
any such phenomenon. There was no tendency to any special eleva-
tion of blood sugar after it had been lowered by exercise, neither was
the lowering due apparently to mere delay in the absorption of food,
for the blood sugar remained lower at 8 p.m. and on the following
morning than after a day of rest.

After the morning experiment of August 21, the diet was abruptly
made almost carbohydrate-free (only 5 gm. in vegetables daily).
The patient continued at rest during the remainder of August 21 and
throughout August 22. The hours of eating were as before. With
this diet, slight but distinct ferric chloride reactions were continually
present, but the blood sugar by the morning of August 23 was found
normal. The graphic chart (Chapter III) shows some of the data,
but omits the 30 gm. glucose which were taken on 4 days as follows:

August 23, the patient exercised 10 to 10:50 a.m. as described in
Table II. Between 10:50 and 11 a.m. he ate 30 gm. Merck anhy-
drous glucose. Between 11 and 11 :45 a.m. he did 64 flights of stairs,
and between 11:45 a.m. and 12:45 p.m. 72 more flights, with the
usual walking between. He rested for the remainder of the day.

August 24 was a rest-day. Between 10 and 10:10 a.m. the patient
ate 30 gm. Merck glucose.

August 25, without exercise, the effect of low temperature was
tested, the point being of interest in connection with three questions:
(1) the hyperglycemia caused by cold environment according to re-
ports in the literature; (2) the clinical impression that diabetics do
better in warm weather and chmates than in cold ; (3) the conception
of diabetes as a defect of general metabolism, and the influence of
alterations in total metabolism upon the assimilative function. Ac-
cordingly, at 9:30 a.m. the patient entered a refrigerator room at a
temperature of 45°F., and sat there quietly in a chair until 12:45 p.m.
At 10 a.m. he ate 30 gm. glucose as usual. He was clad in thin
summer underwear, light khaki coat and trousers, thin socks, and
bath;room slippers. The change from the hot summer weather to the
cold room was about as great as could be borne without serious dis-
comfort or danger. The patient maintained muscular rest under
orders. He was uncomfortably chilly, complained especially of cold

TABLE n.
Patient No. 18.

Blood.

Urine
(24 hr.).

J

Date.

5

fi

fk

Corpuscle sugar.

1^

1

E

1

ter
cent

per
cent

per cent

per
cent

per
cent

°F.

Aug. 23 (exercise day) 10:00

0.083

0.083

0.083

102

39.1

0

+++

98.0

a.m.

(calc. 0.083)

10:50 a.m. Ate 30 gm. dex-

0.099

O.IOG

0.097

100

40.5

99.8

trose.

(calc. 0.096)

11:45 a.m.

0.154

0.200

0.143
(calc. 0.094)

. 92

43.6

99.8

12:45 p.m.

0.101

0.111

0.099
(calc. 0.081)

100

39.0

T

99.8

Aug. 24 (rest day) 9:15 a.m.

0.097

0.105

0.068

90

39.0

++

97.6

(calc. 0.077)

10:00 a.m. Ate 30 gm-. dex-

0.097

0.099

0.092

88

36.0

trose.

(calc. 0.094)

10:50 a.m.

0.192

0.222

0.178

—

—

11:45 "

0.170

0.213

0.117
(calc. 0.090)

80

33.0

12:45 p.m.

0.169

0.196

0.170
(calc. 0.123)

81

36.5

Aug. 25 (low temperature)

0.077

—

—

—

42.0

T

++

98.0

9:15 a.m.

9:30 a.m. (entered cold room).

98.3

10:10 a.m. Ate 30 gm. dex-

0.100

0.103

0.095

90

41.6

trose.

(calc. 0.095)

10:50 a.m.

0.164

0.196

0.116
(calc. 0.124)

90

45.0

97.5

11:45 "

0.175

0.196

0.149
(calc. 0.142)

85

38.0

98.0

12:45 p.m.

0.170

0.178

0.152
(calc. 0.175)

85

42.0

97.8

Aug. 26 (exercise day) 9:15

0.091

0.096

0.090

103

40.0

0

++

98.4

a.m.

(calc. 0.082)

10:00 a.m. Ate 30 gm. dex-

0.092

0.092

0.092

103

38.1

99.6

trose.

(calc. 0.092)

10:50 a.m.

0.143

0.156

0.127
(calc. 0.111)

103

34.2

100.0

11:45 "

0.095

0.095

0.095
(calc. 0.095)

100

38.7

100.5

12:45 p.m.

0.052

0.058

0.049
(calc. 0.043)

103

42.0

99.5

2:15 "

0.102

0.121

0.050

80

33.1

(calc. 0.066)

4.77

EXERCISE 473

feet, and shivered slightly toward the close of the experiment. He
was comfortable immediately upon leaving the cold room, and went for
a street-car ride after lunch.

August 26 was another exercise day. After the blood sample was
taken at 9: 15, the patient did 64 flights of stairs, with the usual walk-
ing, up to 10 a.m. Between 10 and 10 : 10 a.m. he ate the usual 30 gm.
glucose. Then, bet?ween 10:10 and 10:50 a.m., he covered 72 flights
of stairs; between 10:50 and 11:45; 72 more flights; between 11:45
a.m. and 12:45 p.m., another 72 flights. He then ate lunch as usual
(12 :45 to 1 : 20) and remained at rest thereafter. An additional blood
sample was taken at 2 : 15 p.m., to give an idea of the behavior of the
blood sugar after eating and rest on an exercise day.

The observations recorded in the table show the following effects of
exercise in this case.

Blood Sugar. — The repression of hyperglycemia by exercise is very
evident. No uniform law of distribution of sugar between plasma
and corpuscles is discernible; if one gains or loses sugar in advance of
the other, the process is not revealed under the conditions of the
experiments.

Blood Volume. — The hemoglobin and hematocrit readings are rather
irregular. It is known that these methods are subject to errors.
Also discrepancies between the two, seemingly not accidental, are a
not unusual experience in carrying out long series of parallel deter-
minations; e.g., at 11:45 on August 23 the percentage of hemoglobin
is diminished and the percentage of corpuscles increased. The im-
pression obtained is that as the individual corpuscles were subject
to change in volume. In general, the hemoglobin readings indicate
slight dilution of the blood with hyperglycemia on August 23, 24,
and 25. An opposite process must be borne in mind; m., the concen-
tration of the blood by exercise, as noted under Table I. These two
processes may be expected to neutralize each other in varying de-
grees, and possibly at the same time to be associated with unknown
changes in the volume of individual corpuscles. The one definite
demonstration is that, as far as hemoglobin and hematocrit determin-
ations can decide, the changes in blood sugar are not accounted
for by simple dilution or concentration of the blood.

Body Temperature. — Slight elevation of temperature, up to 99.8°F.,
was produced by exercise on August 23, and up to 100.5° by the live-

474 CHAPTER V

Her exercise on August 26. In this respect the human experiments
serve as a useful control to those on dogs. Since in the former the
pyrexia is so shght and in the latter so extreme, while the repression
of hyperglycemia and glycosuria is similar in both, the conclusion can
be drawn that elevation of temperature is not the sole or essential
cause of the improved utilization of sugar.

Acidosis. — Though the diet was poor in carbohydrate and rich in
fat, and the heavy exercise must have depleted body glycogen con-
siderably, no acidosis was produced in this diabetic patient to the
extent of any cHnical symptoms or any perceptible change in the ferric
chloride reaction.

The Influence of Cold. — It appears that the environment of 45°F.
raised the blood sugar from 0.077 to 0.100 per cent. Nevertheless it
must be recognized that this level of blood sugar in the cold at 10 a.m.
on August 25 is not significantly higher than that at summer tempera-
ture at 9 : 15 on the previous morning (August 24) . The patient's body
temperature was not appreciabty affected. The differences in blood
sugar after glucose ingestion on the two days are perhaps within the
limits of accidental variation, especially since the possibiKty of a slight
alteration of assimilation by repeated doses of glucose or by the con-
tinuance of carbohydrate-poor diet cannot be wholly excluded. If
any real difference exists, it is in favor of the cold environment, and
might indicate that increased muscular tone, shivering, and the stimu-
lation of metabolism sHghtly facilitated sugar combustion. Though
no harmful effect was here demonstrated, a brief experiment of this
sort in no wise opposes the belief in a harmful influence of cold upon
diabetes.

Observations on Patient No. 34.

This case represented a slightly more severe stage than the preced-
ing, and the tolerance was somewhat lower. The diet consisted of 50
gm. protein, 20 gm. carbohydrate, and 1300 calories, taken in three
meals, 7:30 to 8 a.m., 12:30 to 1 p.m., and 5:30 to 6 p.m. On this diet
there was a decided tendency to hyperglycemia during digestion, as
shown first by the blood sugar of 0.147 per cent at 3:05 p.m. on Sep-
tember 3. On this day a preliminary experiment was performed as
shown in the table, and the marked lowering of blood sugar found at
4:10 p.m. must be attributed to the exercise.

TABLE in.

Patient No.

34.

Blood.

Urine.

Date.

i,

i

§■

Remarks.

i

5 "

Corpuscle sugar.

o
u

per
cent

k

per
cent

u

per
cent

i

mis

per
cent

per
cent

per cent

Sept. 3

Blood taken after

3:05 p.m.

0.147

56.7

111

41.4

0

0

lunch at 12:30

4:10 "

0.100

38.5

111

41.4

p.m. 3:05 to 4:10
p. m. exercised,
climbing 88 flights
stairs, walking
corridors between
times.

S;ept. 12

No exercise; fast-

2:40 p.m.

0.128

0.139
0.121

0,128
(calc. 0.108)

56.7

97

36.1

0

0

day.

Sept. 13

0.105

0.105

52.3

96

36.1

0

0

No exercise.

Before

(calc. 0.076)

breakfast. .

Sept. 14

No exercise.

11:20 a.m.

0.210

0,200

0.180

(calc. 0.228)

50,4

95

35.5

0

0

2:40 p.m.

0.191

0.195

0,191
(calc. 0.184)

95

37.1

5:20 "

0.200

0.195

0.211
(calc. 0.210)

53.8

92

34,0

—

—

Sept. 15

Light work in fore-

11:20 a.m.

0.119

0.118

0.119
(calc. 0,090)

47.6

95

34.0

0

+

noon.
11:20 a.m. to 12:20

12:20 p.m.

0.100

0.103

0,105
(calc. 0,097)

29,0

86

36.0

p.m. Climbed 72
flights stairs and

2:40 "

0.105

0.105

0,102
(calc. 0,105)

42,2

85

37.0

walked as usual.
12 :20 p.m. Lunch.

4:20 "

0.122

0.122

0,122
(calc. 0.125)

50.3

85

32.0

Rested until 1 :50
p.m.

5:20 "

0.100

0.091

0.118

(calc. 0.115)

37.6

86

33.8

1:50 to 2:40 p.m.

Climbed 80 flights

stairs besides

walking.
2:40 to 4:20 p.m.

Rested.
4:20 to 5:20 p.m.

Climbed 88 flights

stairs and walked

in addition.

475

476 CHAPTER V

September 12 was a fast-day. It is seen that the high blood sugar
was still persistent at 2 : 40 that afternoon, but by the following morn-
ing had come down to a high normal level. Marked hyperglycemia
was present on the rest-day of September 14. On the next day after
breakfast the patient was engaged in duties involving light continuous
exercise, and an effect is apparent in the decidedly lower blood sugar
found at 11:20 a.m. Thereafter, heavy exercise reduced the blood
sugar to normal and held it there during the exercise periods, but
during the resting period from 2 :40 to 4 : 20 p.m. the tendency to hyper-
glycemia manifested itself plainly. The most striking feature of the
experiment is the immediate lowering of blood sugar by exercise as
compared with the slow reduction by fasting.

Acidosis. — The trace of ferric chloride reaction which appeared on
September 15 is presumably attributable to the exercise, for this reac-
tion had been negative for over a month preceding on practically the
same diet. The plasma bicarbonate was reduced by exercise on each
occasion. At 12 :20 p.m. on September 15 it was down to 29 per cent,
which is as low as in many patients close to coma; yet the dyspnea was
very transient and the patient entirely comfortable, with none of the
weakness, malaise, and other symptoms generally found in diabetic
acidosis. With rest, the rise of blood bicarbonate was rather rapid
but not immediate; for example, in the period of rest between 2 :40 and
4:20 p.m. on September 15 the CO2 capacity of the plasma rose from
42.2 to 50.3 per cent.

Observations on Patient No. 46.

From the history and graphic chart (Chapter III) it will be seen that
this patient was a frail little man, whose diabetes, though only moderate
in severity, was accompanied by weakness and prostration, more marked
in the subjective feelings than in actual strength tests. Beginning
September 1, this patient fasted (with whisky) through September 5.
On September 6, 3 gm. carbohydrate were given, and on September
7, 6.5 gm. At this point, when the weak patient had been through
practically 7 days of fasting, and glycosuria and acidosis had only
recently subsided, he was subjected on September 8 to a day of exer-
cise to the full hmit of his strength. He could not run rapidly like the

EXERCISE

477

n

a

o

NO (O

"^ ^*

fO

s is

=>!

.d

g

■4-J

3 'ffi

8 s

.>^ "
o

9:40 to 10:50 a.m. Exercise.

10:50 a.m. to 12 m. Rest.

Exercise to limit of strength con-
tinued afternoon and evening.

Total day's work 176 flights
stairs and considerable walking.

1

O

o

o

O

O

o

O

+

+

•mSng

6 °

o

o

O

+

+

+
+

to

CN

1

■spsndi03

per
cent

35.2
43.8
41.0

41.0

1

1

1

1

1

1

1

42.0
42.0
37.0

■mq
-oiSoniajj

per
cent

118
120
117

115

1

1

1

1

1

1

1

On ■«— 1 T-l
O ■^ tH

'00

vol. per
cent

50.0
31.9
39.5

53.8

1

1

1

1

1.

1

1

59.4
42,2
51.3

Corpuscle sugar.

per cent

0.137
(calc. 0.180).

0,143
(calc. 0.136)

1

1

1

1

1

1

1

0.200
(calc. 0.071)

0.143
(calc. 0.117)

0.143
(calc. 0.107)

•jBSns

per
cent

0.154
0.134
0.182

0.166

1

1

1

1

1

1

1

0.371
0.193
0.167

•iBSng

per
cent

0,161
0,139
0.179

0.156

1

1

1

1

1

1

1

0.244
0.161
0.147

.s
a

■IOI[ODIV

gm.
22.5

o
o

o
d

CN

cs

CN

O

d

CN

CN

CN

CN

CS

lO

cs

CN

-XqoqKO

gm.

12.7

en

fa

o

o

o

to

O

NO

o

lO

g

O

•?^£

O

5i

NO

CM
NO

On

On
CN

lO

CD

o

■msjoaj

CO

a ■*

NO

On

O

8

o

g

O

8

O

1— 1

o

d

o

*S3T10|^3

• NO
CO
CN

o
c^

1

ON

8

CN
CN

00
CN

CN

4

Sept. 8
2 :30 p.m.
3:30 "
4:30 "

5:30 "

00
1/3

On

o

(/3

CN

CN

&

PO
CN

4-J

1/3

CN

Sept 25
9:40 a.m.

10:50 "

12.00 m.

478 CHAPTER V

preceding patients, but he plodded faithfully up and down stairs and
by sufl&cient exertion covered a surprising number of flights. The
experiment was useful as a control to those upon diabetics of the sever-
est type, because this patient was as weak as many of the latter. Also,
the effect of marked strain and exhaustion was thus tested. These
have been feared and warned against, as tending to injure assimilation
and create serious danger of coma in patients with anything like a
severe form of diabetes, and it was conceivable that there might be an.
actual influence of these factors, particularly through the nervous
system. Also, from the standpoint of acidosis, it was of interest to
observe the effect of exercise upon a patient who had recently had a
considerable acidosis, whose plasma bicarbonate was still below nor-
mal, and whose glycogen reserves were supposedly depleted by gly-
cosuria and fasting with only a trivial carbohydrate intake.

It is seen in Table IV that during the hour of exercise the blood
sugar fell unmistakably, but in the succeeding hour of rest rose de-
cidedly higher than at the outset. At the end of a second hour of
rest it returned to near its original level. Therefore no benefit is per-
ceptible from exercise at this stage of treatment. If exhaustion was
possibly responsible for the hyperglycemia to any extent, it at least
did no appreciable harm from the standpoint of acidosis. The ferric
chloride reaction was negative. It is not improbable that the traces
present on September 9 and 10 were due to this exercise on September
8. The plasma bicarbonate fell during the hour of exercise from 50 to
3.1.9 per cent, a figure generally indicative of severe acidosis; but there
were no threatening symptoms and no distress beyond that of any very
tired person. The CO2 capacity then rose steadily, until after 8
hours of rest it was 53.8 per cent, or slightly higher than before the
exercise.

Period from September 19 to 25. — In this period the patient was
placed on a fixed ration of protein, carbohydrate, and alcohol, with
daily increase in fat (see graphic chart) . Starting with a total intake
of 1147 calories on September 19, sugar and ferric chloride reactions
were negative. A traceof glycosuria appeared with 1640 calories on
September 21, and increased slightly with 1916 calories onSeptember
22 and 2200 calories on September 23. Then, with 2438 calories on
September 24, heavy glycosuria developed suddenly to the extent of

EXERCISE 479

27.75 gm., and at the same time a faint ferric chloride reaction ap-
peared. On September 25, the fat was still further increased to make
2687 calories, and exercise was employed to the limit of strength.
The purpose of the experiment was to test the effect of exercise upon
such a condition brought on by overfeeding with fat.

As shown in the table, there was a remarkable drop in glycosuria,
down to 2.77 gm. The blood sugar fell in the exercise period 9:40 to
10:50 a.m. from 0.244 to 0.161 per cent, and then on resting till 12 noon
fell further to 0.147 per cent. The patient was slightly stronger than
before, but the factor, of overstrain was still present. This in itself
seemed to have no demonstrable importance. The initial blood sugar
was higher than on September 8, but this was merely incidental to the
diet. The actual diabetic condition was better in consequence of the
longer treatment. The better assimilation was indicated by the far
greater fall of blood sugar during exercise, and by the continued dimi-
nution during rest.

In Table IV, as in Table III, the hemoglobin and hematocrit figures
permit no uniform interpretation, aside from the fact that the changes
in blood sugar are not accounted for by changes in blood volume so far
as these methods can reveal. Also it is not possible to distinguish
any rule governing the distribution of sugar between plasma and
corpuscles.

Though the condition had been produced by feeding fat, and the
exercise presumably depleted the carbohydrate supply, there was no
appreciable tendency to acidosis. The existing faint ferric chloride
reaction was unchanged. The fall in the plasma bicarbonate from
59.4 to 42.2 per cent during the exercise period 9:40 to 10:50 is no
greater than ordinary, and in the rest period up to 12 noon there was a
rise as usual, up to 51.3 per cent. The patient recovered easily from
his weariness and experienced no unpleasant symptoms.

The impression is given that the condition created by excessive
calories was in large measure relieved by the increased combustion
due to exercise. It is evident also that the same patient can react
differently to exercise at different stages of treatment.

480 CHAPTER V

Observations on Patient No. 2.

This patient was an Italian girl aged 17 years, whose diabetes at
the time of these observations was somewhat more severe than any of
the preceding cases. At the same time her strength was such that she
could carry on heavy muscular labor continuously without difi&culty.
Two new features were tested here : (1) a comparison of fast-days with
and without exercise in a case of this severity; (2) the effect of heavy
exercise upon the tolerance over a long period of time (8 months).

First may be mentioned the comparison of the two fast-days, Septem-
ber 12 and 16. The former was a day of practically no exertion. It
may be that the sUght activity and excitement of the street-car ride
and visit were responsible for the slightly higher sugar in the afternoon,
immediately after returning from the trip, as compared with the fore-
noon. The blood and plasma sugars before breakfast oii September
13 were practically identical with those on the morning of September
12, showing no perceptible influence of the single fast-day toward re-
ducing h5^erglycemia. The regular diet being slightly in excess of the
true tolerance, the plasma sugar on the morning of September 16 had
reached 0.172 per cent, as compared with 0.139 per cent on September
12. It is observed that exercise on this day was effective in reducing
the h3rperglycemia, to 0.151 per cent in plasma at 10:50 a.m. and to
0.120 per cent at 12 : 10 p.m. But the patient bore the exercise on this
fast-day badly, and was compelled to sit or lie down the entire after-
noon. The sugar then rose to 0.128 per cent at 3:50 p.m. and to the
notably high level of 0.220 per cent at 5:10 p.m. The symptoms of
weakness and dizziness were characteristic of acidosis, and this was
verified by the CO2 capacity of the plasma. This fell as usual during
the heavy exercise between 9:15 and 10:50 a.m., and rose somewhat
as usual during the lighter exercise up to 12 : 10 p.m'. Then, instead of
rising with rest, it continued to fall as the blood sugar rose, so that at
5:10 p.m. the plasma bicarbonate was only 40 per cent. After a
night's rest, however, it was found on the next morning that matters
had adjusted themselves. The blood sugar was distinctly lower and
the plasma bicarbonate a trifle higher than on the morning of Septem-
ber 16. There had been a temporary upset from the exercise; in
particular, this patient's usual tendency to acidosis on fa-st-days had

EXERCISE 481,

been increased; but the final outcome of the fast-day with exercise was
a diminution of hyperglycemia, while a fast-day without exercise had
not reduced hyperglycemia. It cannot be supposed, however, that
this effect upon the blood sugar was worth the disturbance and risk
under the conditions.

Turning to the general and prolonged features of the experiment,
it can be seen by reference to the patient's graphic chart (Chapter III)
that between May 27 and July 24 she was on a carbohydrate-free diet
of 1500 to 1800 calories. This was in excess of the tolerance, for
ferric chloride reactions were almost continuous and glycosuria alto-'
gether too frequent. The plasma sugar of 0.208 per cent on the
morning of the fast-day of July 25 may be taken as typical of the
hyperglycemia produced by this diet. After the carbohydrate toler-
ance test which ended August 9, carbohydrate-free diet was resumed
with 1400 to 1600 calories daily. Again on September 4, it is seen in
the table that the plasma sugar was 0.238 per cent. The patient per-
formed moderate exercise for an hour, then rested 15 minutes; there
was a very marked reduction of sugar, to 0.152 per cent in the plasma.
No discomfort or acidosis symptoms resulted, and any lowering of
plasma bicarbonate during the moderate exercise was corripensated in

15 minutes of rest, for the carbon dioxide capacity was the same at
12:30 as at 11:15.

Thereafter the comparison of the two fast-days of September 12 and

16 was carried out with the results above described. The acidosis
resulting on a fast-day in contrast to a feeding day may again be
mentioned.

Another feature was incidentally noticed, the significance of which is
unknown. On September 17 the patient weighed 38.3 kilograms
without edema. With the beginning of heavy exercise on that day,
there was an immediate rise in weight to 40 kilograms on September
18, with marked visible edema of face and ankles. The edema passed
off within a few days and the weight remained approximately what it
was before. It will be observed in the table that the hemoglobin and
hematocrit readings after September 17 showed a fall decidedly beyond
any possible experimental error, and the former values were not re-
gained until September 29. In other words, the blood appeared to be
diluted during the period of edema. Accidentally or otherwise, the

482

CHAPTER V

id climb-
0 break-

climbing
lorridors.
;orridors.
sted and

!:15 p.m. Exercise
Iking corridors,
p.m. Rested. Ni
.1 12:30 p.m.

1
o

e

m. Exercised by
rs and walking c
10 p.m. Walked c
er of day, exhaui

&

"3

rsi '"3 CO

.a|

10:50 a.
ghts stai
.m.tol2:

remaind

.m. t
tairs,
0 12
first

ca m +' ..

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2 .a ca -g g>

>r> M •r> M

ii C3

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■a a

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^

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0

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<N

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s

lO ID

vd

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CO ^ CO

Ov

^*

CO

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00 00

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10

EXERCISE

483

1

1

1

Blood taken after breakfast and 32
flights stairs; has exercised large part of
each day since Sept. 17; 33 flights
stairs.

13
(A

bo

a .

■^&

S 2

Blood taken after 32 flights stairs; 25
gm. carbohydrate in wheat flour added
to lunch; 32 flights stairs and 60
blocks walking between lunch and
4:45 p.m.

B

1

s °

fl
|i

1

-4-J

a

1

o
5!

o

CO
CO

o o

CN CN

CO CO

"1

00
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1

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s

t-

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oo 00

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1

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d

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CO

d

d

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d

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484

CHAPTER V

1

n

1

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■d

o

1

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11 1

1

1

1

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il 1

1

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1

1

1

■''OD

voL
per
cent

49.9

o

00

CN

CO

CO

•*
^

00

1/^

■*

^

00
CN

CS

00

i

i
1

1 1

1

1

1

1

1

1

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1

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1

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1

1

•«3ns

11 i

d

s

CO

d

00

d

00

o

CN

d

d

g

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d

CN
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d

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d

to
to

CO

d

00
CN

d

CN

d

o

CN

d

CN

d

d

CN

d

CN
CN

d

•TCSng

per
cent

0.322

s

CM

d

CO

fO
ro

d

d

00
CN

d

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o

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d

b

d

CM
CN

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CM

d

6

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Nov. 5

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Q

EXERCISE 485

edema was coincident with the beginning of exercise. The changes in
hemoglobin and corpuscles were not parallel to alterations in the sugar
concentration. There have been no other observations on diabetic
patients to indicate whether the blood volume is ordinarily increased
in the period of edema to which such patients are often readily subject.
The regular diet through this time remained at 1450 to 1600 calories.
After September 16, increasing exercise was carried out daily as the
patient's endurance improved with training. Only on fast-days
moderate exercise or none at all was required. It is seen in the table
. that on September 17, after walking, the blood sugar on this same diet
was lower than it previously had been, without exercise. On Septem-
ber 21, after heavy exercise, it was lower still. On September 22, it was
the lowest yet observed. On September 25, with the blood sugar
approximately normal (0.118 per cent) just before lunch, the experi-
ment was performed of adding 25 gm. carbohydrate in the form of
wheat flour to the noon lunch. Although this patient had previously
been subject to repeated glycosuria on carbohydrate-free diet with the
same protein and total calories, glycosuria remained absent with this
quantity of carbohydrate with heavy exercise, and the plasma sugar
at 4:45 p.m. was only 0. 162 per cent, in contrast to the above mentioned
values of 0.208 and 0.238 per cent observed on fasting before exercise
was inaugurated. The use of carbohydrate was continued, but the
form was changed to green vegetables. On September 29, with 25
gm. carbohydrate in the diet, and after breakfast had been taken about
7:30 a.m. as usual, the plasma sugar at noon was 0.128 per cent. The
hyperglycemia of 0.357 per cent in the plasma on Octobei: 29 was the
result of the carbohydrate tolerance test at that time, with 140 gm.
carbohydrate in the diet and glycosuria present. The diet up to this
time had involved slight undernutrition, especially in view of the
exercise. This was evidenced by the weight, 41 .3 kilograms on June
27, 40.4 kilograms on October 30. After October 30 the carbohydrate
allowance was diminished to 10 gm., and the attempt was made to
build up weight by steady increase of total calories. The exercise at
the same time was pushed to a maximum, with the idea that the patient
might be made to lose fat while building up her muscles to the greatest
possible size and functional power on a diet abundant in protein and
total calories. Her day's work frequently consisted of 200 flights of

486 CHAPTER V

stairs, walking 75 blocks, 30 minutes roller-skating, and 30 minutes
hard work with the medicine ball. In addition she carried on minor
activities, so that she was fully resting only during the hours of sleep.
The strength was greatly increased by this program. The patient
had the full strength and endurance of the most vigorous working
girl and could outdo the average normal girl. It is evident from
Table V, however, that the attempt thus to use exercise to compensate
for an excessive caloric ration was a failure. As the calories were
increased, the blood sugar rose in proportion, and the rise was not
checked by omitting all carbohydrate after November 24. Glycosuria
also became rather frequent, as shown in the graphic chart. The ulti-
mate outcome was that the patient was dismissed on February 2, 1916,
weighing only 39.2 kilograms, on a carbohydrate-free diet of 75 gm.
protein and 1500 calories; i.e., a reduction in both weight and food.
No blood sugar analyses were performed later than January 15, but in
view of the glycosuria present as late as January 29, it is certain that
hj^erglycemia was persistent.

Reference may be made also to the three formal tests of carbo-
hydrate tolerance performed during this period (July 26 to August 9,
October 11 to 30, December 13 to 20). The point to be determined
was whether the building up of the muscles in mass and function
would bring about any noteworthy improvement in the carbohydrate
tolerance. It was clearly evident that the patient gained in size and
power of her muscles, but it is also evident from the history and the
graphic chart that the carbohydrate tolerance by accurate tests re-
mained unchanged. In addition, it can be observed from the graphic
chart that the attempt to introduce as much as 30 gm. carbohydrate
in the diet in January was borne for a few days by virtue of hard exer-
cise, but terminated in marked glycosuria. The tolerance meanwhile
was injured, since glycosuria resulted thereafter from smaller quanti-
ties of carbohydrate, so that on January 26 to 29 glycosuria was pres-
ent on diets of 77 gm. protein, 25 to 0 gm. carbohydrate, and 1200 to
1400 calories.

The behavior as respects acidosis is also of interest. Some of the
fluctuations in the plasma bicarbonate in this period, shown particu-
larly in the graphic chart, were due to exercise. In general this curve
remained close to the lower border of normal. The ideas concerning

EXERCISE 487

the carbohydrate supply and the glycogen reserve as governing acidosis
are so firmly intrenched in the literature that attention may profita-
bly be called to these results with prolonged heavy exercise on diets
always poor in carbohydrate and completely free from carbohydrate for
months at a stretch. The ration of approximately 100 gm. protein
could furnish approximately 60 gm. potential carbohydrate, but it is
known that normal persons generally exhibit more or less acidosis, at
least temporarily, when placed upon diets of this character. Two ques-
tions maybe raised. First, what effect will exercise haveuponthe acid-
osis of carbohydrate-free diet? Second, if the introduction of carbohy-
drate into the diet is made possible by exercise, will this carbohydrate,
which is consumed by the exercise, have the usual effect in diminishing
acidosis? Contrary to some existing preconceptions, it will be seen that
exercise produced no perceptible tendency to acidosis, except on the
fast-days as above mentioned. The evidence on the point is as fol-
lows: (a) Practically continuous ferric chloride reactions had been
present throughout the earlier months in the hospital. They were
■ thus present on the carbohydrate-free diets of 1600 calories or more
prior to August, and on the lower carbohydrate-free diets, viz. about
1500 calories, they had ceased in September, shortly before exercise was
begun. Exercise did not bring back such reactions; on the contrary,
they were negative or limited to indefinite traces on the carbohydrate-
free diet of 2500 calories, November 24 to December 4, and entirely
negative on the carbohydrate-free diet of 2000 calories December 6 to
11. There was thus if anything a diminution of ferric chloride reac-
tions after exercise as compared with the period before exercise. (&)
The data for ammonia nitrogen are best seen by a glance at the graphic
chart. It is evident that the ammonia determinations after Decem-
ber 2 show no striking tendency to acidosis as compared with those
before June 25. The question of the usefulness of carbohydrate
in lowering acidosis during exercise cannot be answered from the data
in this record. With the same number of calories in the diet there is
no essential difference in the ammonia excretion on December 31 and
January 6 with 30 gm. carbohydrate and on January 15 without
carbohydrate, but here the proper utilization of the carbohydrate is
made questionable by the glycosuria and marked hyperglycemia.

488 CHAPTER V

B. The Efpect upon Carbohydrate Tolerance and Glycosuria.

It was noted in several of the above studies that glycosuria was
either prevented or checked after it had begun, and this rule applied
also to the glycosuria resulting from carbohydrate-free diet or (patient
No. 46, Table IV) from simple addition of fat to a diet.

From the standpoint of clinical experience, patients may be divided
into three groups on the basis of their reaction to exercise: I, those
showing more or less improvement in food tolerance; II, those show-
ing little or no change in tolerance; III, those in whom the effect is
injurious.

I. A number of tests were performed of which the following is typi-
cal. Patient No. 34 (see Table III above; see also graphic chart.
Chapter III) was started on a carbohydrate tolerance test on Octo-
ber 11. With a steady increase of 10 gm. daily in the carbohydrate
intake, glycosuria appeared with 200 gm. carbohydrate on October
28, and increased slightly with 210 gm. carbohydrate on October 29.
The patient had been at rest up to this time. The daily increase of
carbohydrate was continued, but exercise was imposed in the form
of 72 flights of stairs and 30 minutes lively rope-jumping daily. The
glycosuria ceased immediately, and reappeared only with 260 gm.
carbohydrate on November 3. A similar observation is described in
the history of patient No. 49. This improvement in tolerance belongs
to the milder cases, and may practically be said to vary with the
degree of mildness. It is well known that diabetics of milder type
than those represented in this series may assimilate much larger quan-
tities of carbohydrate with exercise than without, and this fact has
been counted as an advantage in the dietetic management of patients
of the poorer class, who must live by hard manual labor. As was
shown above (patient No. 46, Table IV) the reaction to exercise
varies with the time and degree of treatment. Patients with active
diabetes may show no improvement of assimilation, and only injuri-
ous and perhaps dangerous consequences from exercise, but later,
after a sufficient period of sufficiently thorough treatment, may reach
the condition in which exercise is clearly beneficial.

II. Patient No. 26 (see graphic chart, Chapter III), a girl of 14
years, began a carbohydrate tolerance test on October 6. A trace of

EXERCISE 489

glycosuria appeared with 130 gm. of carbohydrate on October 19.
Exercise was then introduced in the form of stair-climbing and rope-
jumping to the point of exhaustion daily. The glycosuria continued,
and increased sUghtly on the ensuing days up to October 23 as the
carbohydrate was slightly increased. Even with exercise, two par-
tial fast-days (October 24 and 25) were necessary to abolish it. This
instance is typical of cases in which exercise shows no appreciable
effect upon the tolerance one way or the other.

Patient No. 43 (see graphic chart, Chapter III), a young woman of
27 years, beginning August 1, 1915, took a diet of 100 gm. carbohy-
drate and 2150 to 2500 calories. On this she remained free from gly-
cosuria during the week ending August 7. In the following week
(August 9 to 14) she was sent on long walks, as much as 8 miles
daily, which, though taken slowly, were enough to tire her thoroughly.
On August 10 and 11, she happened to have crying spells which brought
on glycosuria. A walk was taken immediately after the one on
August 10, and it was found that the urine became immediately free
from sugar. Nevertheless glycosuria recurred from time to time
subsequently; viz., on August 19 to 20, 23 to 25, and September 11.
After the fast-day of "September 12 exercise was temporarily discon-
tinued, to determine the effect of the omission upon the tolerance.
Traces of glycosuria occurred on September 14 to 15.

On September 16, blood was taken at 9:15 a.m., as shown in Table
VI. The patient then ate breakfast and went for a walk of 54
blocks. The marked rise in blood sugar found upon her return at
12:20 p.m. may be attributable to the breakfast; the walking had not
availed to prevent this increase of hyperglycemia. The hemoglobin
and hematocrit readings seemed to indicate that the exercise was
sufficient to concentrate the blood appreciably. Notwithstanding
the hyperglycemia, however, the glycosuria which had been present
on the two previous days ceased promptly with this exercise, and re-
mained absent as exercise was continued on the succeeding days.
The data do not permit decision whether the cessation was due to a
simple diminution of renal permeability or (as is more probable) at
liqast partly to a slight lowering of blood sugar (as compared with
corresponding hours on the preceding days, when no analyses were
made).

490

CHAPTER V

In the 3 weeks between September 19 and October 10, severe exer-
cise was discontinued, and the patient took only a short walk daily.
Nevertheless glycosuria was fully as rare as before,' the only trace in
this period being on the last day. Mild exercise was employed dur-
ing the carbohydrate test, October 11 to 30, and, as evident from the
graphic chart, the assimilation was not quite so high as shown in the
previous test in July. The slight difference between the tests may be
attributed to the unduly high diets of the intervening period. It is
evident that exercise failed to build up the tolerance or to prevent
the injury resulting from such diets. On the whole, the influence of

TABLE VI.
Patient No. 43.

Blood.

Urine (24 hr.).

Date.

Sugar.

Plasma

sugar.

Corpuscle sugar.

CO2

Hemo-
globin.

Corpus-
cle.

Sugar.

FeCli
reac-
tion.

1915
Sept. 12, 11:30 a.m.

per cent
0.154

per cent
0.154

per cent

0.154

(calc. 0.154)

per cent

37.1

percent
101

per cent
46.0

gm.
0

0

Sept. 16,9:15 a.m.
12:20 p.m.

0.167
0.185

0.164
0.188

0.137
(calc. 0.173)

0.147
(calc. 0.180)

39.2
42.0

88
95

33.0
38.8

0

0

exercise upon the tolerance of this patient was so slight as to be
barely recognizable.

Occasional ferric chloride reactions were present both before and
after the inauguration of exercise. Their occurrence was not gov-
erned solely by the quantity of carbohydrate in the diet, as may be
seen by comparing the periods July 27 to 31, August 26 to 28, and No-
vember 7 to 25 in the graphic chart. Exercise had no perceptible
influence in this respect. The plasma bicarbonate is seen also to hold
generaUy a normal level. Nothing can be concluded beyond the fact
that exercise failed to produce any appreciable tendency to acidosis,
and as far as carbohydrate served to prevent acidosis, it was appar-
ently as effective with exercise as without.

EXERCISE 491

III. No observations have been recorded which show the injurious
effect of exercise in patients with the severest diabetes. The injuri-
ous effect easily demonstrable in cases even of milder type under
inadequate treatment is, as above mentioned, another matter. The
carbohydrate tolerance of the patients properly belonging in this
group is practically nil, even under the most rigorous treatment.
Their tolerance for protein and total calories is likewise excessively
low. Experience has clearly and repeatedly demonstrated that their
tolerance cannot be built up by exercise. Experiments such as de-
scribed in patient No. 46 (Table IV above) will have different and
sometimes dangerous results if performed upon these severest cases.
In view of their great proneness to glycosuria, it is a difficult matter
to show conclusively that a given patient of this type has glycosuria
on exercise, and is free from glycosuria at rest. The existing evidence
is of two kinds:

(a) The demonstrable changes in the blood sugar, which can be
shown to be increased instead of diminished by exercise, as above
mentioned.

(b) The general clinical experience that patients of this sort are
badly affected by heavy exercise. They are weak and worn out, nerv-
ous and unwell on even moderate exertion. Those with diabetes
even of a somewhat milder type sometimes reach this condition tem-
porarily when they overdo exercise without supervision. Such pa-
tients have been treated with complete bed-rest for periods of one to
several weeks continuously, and the effect of such rest has been good,
certainly upon the general health and seemingly also upon the
tolerance.

C. The Use of Exercise in Various Classes of Patients.

From the standpoint of practical usefulness, the experience with
exercise in the present series of diabetic cases may be expressed by
grouping patients into the following six classes.

1. It is obvious that some patients are received in very critical
condition and die before there can be any possible use of exercise.
There were six such cases in the present series; viz., Nos. 11, 15, 30,
38, 45, and 71.

492 CHAPTER V

2. Exercise is necessarily limited or impossible in the youngest and
the oldest patients, also in those with organic disability of some

■kind. In the present series, Nos. 55 and 68 were infants too young
for any considerable exercise, and not much was possible for patient
No. 73, a girl of 3 years, already weak with advanced diabetes. Senile
patients have, as a rule, not been taken. Therefore patient No. 17,
with arteriosclerosis and tendency to gangrene, and No. 58, senile
and nearly blind, are the only ones falUng in this category. The only
ones exempted from exercise for complicating disease were patients
Nos. 25 and 61, whose cardiorenal conditions were far more serious
than the diabetes. Milder disabilities in other patients have not
prevented prescribing exercise in keeping with their capabilities.

3. Exercise is sometimes inadvisable, as mentioned, because of the
actual severity of the diabetes. In the great majority of cases this
applies only to a transitory stage, and under proper treatment exer-
cise later becomes feasible. The cases in this series which were too
severe for the use of any important amount of exercise from the time
they were received, are Nos. 8, 54, 69, and 75. A number of other
patients in the series have shown downward progress, so that they have
finally reached this stage in which exercise is impracticable on account
of the severity of the diabetes and the accompanying weakness. In
some instances at least this downward progress has been due to the
wrong use of exercise in an attempt to maintain the patients at higher
strength and on higher diets than advisable. Both children and adults
are deficient in muscular power and disincHned to exertion on the
minimal diets required for the severest diabetes, and obviously neither
diet nor activity should be forced in such cases.

In contrast with these three classes stand three other more numer-
ous classes in which the clinical results of exercise have been gratifying.
Nearly all these patients are of the type in which exercise is impossible
or injurious under former methods of treatment. One thing accom-
plished by the present dietary method has been to make available the
benefits of exercise to the large number of patients of this group. The
effects upon the general health are far more important than the influ-
ence upon the tolerance.

4. First may be mentioned its use in the great mass of severe cases
in adults. Exercise was not employed for patient No. 1, and she was

EXERCISE ^ 493

clearly the worse for having been kept at rest, according to the
former traditions for this type of case. She is included in the group
suitable for exercise, which also comprises cases Nos. 2, 3, 5, 6, 7, 9,
10, 14, 16, 18, 19, 20, 22, 24, 27, 29, 31, 32, 34, 36, 37, 39, 40, 43, 44,
47, 48, 49, 50, 52, 56, 59, 67, 70, and 74. For this large body of pa-
tients, exercise is the most powerful deliverer from ennui, depression,
neurasthenia, and invaUdism. . Exercise and fresh air make the most
of whatever strength is possible under the conditions of the disease,
and doubtless aid in raising resistance against intercurrent infection.
In contradiction to the fears of those who hesitate to employ diets as
low as the tolerance requires, the contrast between patients con-
fined and stufEed with fat under former methods, and those with re-
stricted calories and the benefits of exercise and outdoor freedom, is
manifestly in favor of the latter with respect to immunity from com-
pUcations and comfort and efl&ciency in all respects.

5. Most cases of diabetes in children are distinctly benefited by
exercise on a diet which makes this possible. Such are cases Nos.
4, 13, 26, 28, 42, 51, 53, 62, 63, 64, 66, 72, and 76, in the present
series. It means much to a child to be able to indulge in active
play, especially outdoors. When growth and development are pos-
sible at all, these are doubtless aided by healthful exercise. Even
when they are impossible, on account of the severity of the diabetes,
the child's looks, spirits, and attitude toward life have been improved
by active play within the limits of easy endurance.

6. Perhaps the greatest usefulness of exercise has been manifested
in a group of milder cases. This applies theoretically to cases such
as Nos. 40 and 65, on account of their mildness; but the group par-
ticularly referred to comprises certain middle-aged or elderly patients,
including those with obesity. Graduated exercise, sometimes carried
to a high point, has proved beneficial not merely in raising the
carbohydrate tolerance, but also in correcting invalid tendencies asso-
ciated with advancing years or sedentary habits. Patients Nos. 35
and 41, though sound in wind and limb, were drifting toward invaUd-
ism, and when the diabetes was brought under control by diet, exer-
cise aided materially in restoring them to normal life. Patient No.
12 was elderly, sedentary, poor, and seriously debihtated. Rigid
undernutrition was necessary to control his diabetes. Exercise and

494 CHAPTER V

fresh air, combined with undernutrition, gradually restored his
working power. He was one of the obese group. In other patients,
such asNos. 21 and 57, exercise was obviously an aid in controlling the
tendency to obesity, and thus benefiting both the diabetes and the
general health. Though such patients are better off in all respects
if they can really carry on exercise" successfully, a question frequently
met is how far complicating ailments contraindicate exercise. Pa-
tient No. 46 had slight arteriosclerosis and large double inguinal
hernia, but nevertheless proved able to perform moderate exercise,
especially in the form of regular walking. Though it did not save
him from a final pulmonary infection, it was evidently beneficial as to
comfort, strength, and resistance. Patient No. 33 presented the most
doubtful problem, for she had blood pressure of 190 mm., uterine
hemorrhages, and a variety of complaints suggesting organic disease.
With these, she was fat and flabby, with the usual relaxed abdomen
and neurasthenic disposition. It was decided to make a trial of
exercise, and as shown in her history, the ultimate outcome was good
in all respects. The tolerance was raised, the obesity and neuras-
thenic troubles were reheved, and even the blood pressure returned to
normal with the general improvement. It is believed that in this
case exercise was of decisive importance, and that the psychic factor
would have precluded success from purely dietetic management.
Obviously this policy and result would have been impossible in the
presence of serious organic disease. Exercise was carried to its
highest point in patient No. 23. He has been turned into a real
athlete, and subjectively has enjoyed the best health of his life.
Exercise to this degree must be considered inadvisable for the great
majority of patients.

In summary, exercise has been impracticable because of acute
terminal conditions, complicating factors, or severity of the diabetes
and bodily weakness in altogether 17 patients of this series. In the
other 59 cases exercise has found some place in the treatment at earUer
or later stages, and has been beneficial when properly employed.

EXERCISE 495

D. The More Permanent Effects of Exercise upon Assimila-
tion AND THE Diabetic Condition.

The question of exercise has possessed considerable practical and
theoretical interest in connection with the conception of diabetes as a
weakened function involving the total metabohsm, rather than the
mere utilization of carbohydrate. From this standpoint the transi-
tory reduction of glycosuria and hyperglycemia by exercise is of minor
importance. The two chief theoretical aspects of the problem and
their practical applications may be stated as follows :

1. One question touches the relation of the pancreas and the
muscles as the two factors chiefly involved in the combustion of sugar or
other foods. Combustion being deficient because of deficiency of the
pancreatic factor, the question is to what extent this deficiency can be
compensated by increasing the muscles in mass and function. The
answer furnished by the present series of observations is that the
apparent compensation actually runs parallel to, and is governed by,
the strength of the pancreatic factor alone. With milder diabetes, the
organism still possesses a conside'rable metabolic capacity. Combus-
tion of sugar is accelerated in correspondence to the increased needs
of the muscles in a manner more or less similar to the condition in
health, and the apparent carbohydrate tolerance is thus increased.
As the pancreatic function falls more and more below the normal, the
response to exercise diminishes in proportion, until the point is
reached at which no perceptible alteration of carbohydrate tolerance is
possible. In more severe diabetes, the increased mobilization of
food substances resulting from exercise is greater than can be provided
for by the feeble pancreatic fxmction, and injury is evident in the in-
crease of both sugar and acetone bodies. These more severe states in
which lack of benefit or actual injury by exercise occurs may be tran-
sitory or permanent. In the former instance the pancreatic function,
which under improper diet is unable to respond to exercise, may be
considered to be strengthened by suitable treatment, so that exercise
later proves beneficial. The essential points at issue were the follow-
ing: (o) With a given pancreatic function, is there a specific improve-
ment of food assimilation with increased mass and function of the
muscles? The answer from these observations is that food combus-

496 CHAPTER V

tion is accelerated and increased in proportion as the power of com-
bustion is retained, but there is no evidence of specific improvement
in this power, (b) Will the increased mass and activity of the mus-
cles, through hormone or other agencies, stimulate the pancreas in
such manner as to increase its internal secretion, thus strengthening
the deficient pancreatic factor? The general result of the observa-
tions speaks against any demonstrable influence of this character.

2. If the entire metabolism is affected in diabetes, and injury re-
sults from feeding all classes of foods beyond the tolerance, the ques-
tion arises how and why this injury is produced. Is every increase of
total metabohsm injurious? If so, exercise must in the long run be
injurious. On the other hand, does the injury possibly result from the
burden of an excess of food substances present, either stored foods
such as glycogen, protein, or adipose tissue, or circulating foods, as
represented by the hjrperglycemia and h3^erlipemia of diabetes? In
this case exercise, by reducing bodily reserves and also relieving the
glut of mobilized materials, may act in a truly beneficial manner on the
same principle as fasting. Exercise could to some extent serve as a con-
venient and agreeable substitute for fasting and reduced diet, the pa-
tient keeping down his weight and his blood sugar while taking a more
satisfying diet and maintaining a higher degree of physical efi&ciency.
The question may be otherwise put as follows: If a diabetic patient
can tolerate a given diet, is it permissible to increase this diet by a
given nmnber of calories while taking care to bum up these added
calories by exercise? Will the condition thus be the same as though
the extra food had not been taken, or will injury still be produced by
the increased metabohsm? Present experience with both patients and
animals indicates that neither of the two extremes represented in these
questions is correct. Even in the cases where exercise acts favor-
ably it can be shown, as in the prolonged study of patient No. 2
(Table V), that even the heaviest exercise caimot atone adequately or
permanently for a high diet. Such use of exercise has proved disas-
trous in every case in which it was attempted in the present series.
This fact is illustrated in cases such as Nos. 2, 32, 36, 37, 39, 42, 47,
and others. In many of these cases it will be noted that the blood
sugar could not be made or kept normal by even the heaviest exercise.
In other cases, such as Nos. 37 and 42, the blood sugar was brought to

EXERCISE 497

normal on liberal diets, and the patients were normal to the routine
tests for considerable periods. Nevertheless hyperglycemia and
other symptoms returned later, and the end result was fatal. On
the other hand, the use of exercise has not proved harmful, except in
the few severest cases mentioned. In cases of decidedly mild char-
acter, exercise, by keeping down weight and improving tolerance,
may serve to a limited degree as a substitute for fasting and reduced
diet. It has thus been used with benefit in the group of elderly pa-
tients above mentioned. Nevertheless, histories such as those of
patients Nos. 23 and 41 show that even in these milder cases exercise
is limited in its usefulness in the long run, and restriction of total ca-
lories must always be the essential reliance for the permanent control
of hyperglycemia and other symptoms. The general conclusion on
the questions mentioned may be expressed as follows. The greatest
and most rapid injury from excessive diet occurs when weight and
food materials are allowed to pile up without restraint. Exercise, by
reducing weight and food accumulation, diminishes this injury, and
the relief is genuine to this extent, even though obtained at the price
of increased metabohsm. Nevertheless the burning up of surplus food
by exercise is not equivalent to withholding such food, and in severe
cases the diastrous result is merely delayed and not prevented.

Though exercise cannot atone for thfe damage of excessive caloric
feeding, it apparently can make possible the use of a higher propor-
tion of carbohydrate in suitable cases. Its well known power of
diminishing glycosuria and hyperglycemia can probably be used for
this purpose without injury, provided only the total calories are kept
sufiiciently low. Further information concerning the effect on acidosis
when carbohydrate is thus used would be of interest, but with a suit-
able caloric intake acidosis is a matter of only minor practical im-
portance. The disappointment of the hope that exercise might per-
mit of higher diets and correspondingly higher bodily efficiency in
severely diabetic pa,tients is of practical importance for the treatment,
especially of paltierits of the poorer class. Repea^tedly in the present
series the attempt has been made to build up such patients so that
they could work with maximum efficiency. The final result has always
been disastrous, no matter how well the patient might seem to thrive
for the time being on high diet with the aid of exercise. It may be

498 CHAPTER V

urged that such pati'ents must work to make their living, and require
high diets for this purpose. A comparison with cardiac disease is
proper. A patient with mild diabetes, like the one with mild heart
trouble, may carry on more or less manual labor without injury. The
patient with more severe diabetes is as unfit for heavy manual labor
as the corresponding cardiac patient. As long as there is no cure for
d abetes, such patients must necessarily conduct themselves as sick
persons and not as well persons, and financial conditions should be
adjusted accordingly, with public aid if necessary. Granting a suit-
able low diet, diabetics in general, with the comparatively uncommon
exceptions mentioned above, are benefited by healthful exercise within
the limits imposed by the diet. In the preliminary communication
concerning exercise,^ warning was given against its use as a sub-
stitute for dietetic measures, and this warning has been justified
by the more prolonged experience. On the other hand, the benefits to
the strength, spirits, and general health have also been substantiated,
and it would be a gloomy prospect to return to the former practice of
strict rest for severely diabetic patients. In the final outcome, over-
strenuous or exhausting exercise in the endeavor to build up a true
increase of tolerance has been abandoned, and muscular activity has
been employed within the easy limits of strength for its beneficial
influence upon the general health and spirits of the patients.

Conclusions.

1. The diminution of glycosuria and hyperglycemia by exercise de-
scribed by former authors in milder diabetes has been found to obtain
also in more severe cases under suitable dietetic management. In
cases of still more severe type, this effect of exercise may be lacking,
and the blood sugar and general condition may even be affected
injuriously.

2. In suitable cases the effect of exercise in diminishing glycosuria
and h)^erglycemia is demonstrable when these have resulted from
the addition of fat to the diet.

3. No appreciable tendency to acidosis has been produced by exer-
cise under the ordinary conditions of proper dietetic management.

lAUen, Boston Med and Surg. J., 1915, clxiii, 743-744.

EXERCISE 499

A distinct tendency to acidosis may be produced in patients inade-
quately treated by diet, or in the severest cases, or sometimes on
fasting or very low diet. Under such conditions exercise must be used
with caution.

4. No special relation has been observed between the changes in
blood sugar concentration produced by exercise and the blood volume
(as judged by hemoglobin and hematocrit readings) or the distribu-
tion of sugar between plasma and corpuscles.

5. Exercise may perhaps be useful as a means of introducing a higher
proportion of carbohydrate in the diet in some cases, but cannot serve
as a substitute for total caloric restriction in cases at all severe in
character.

6. Most of the cases in which exercise has been beneficially em-
ployed in the present series are of a grade of severity which pre-
cluded the use of exercise under former methods of treatment. The
present dietetic management has served to make available the bene-
fits of exercise to this numerous group of patients. At the same time
the observations carry a warning against the abuse of exercise even in
milder cases, whenever an undue total caloric burden is thereby in-
volved. In the final outcome, muscular exercise and development
have exhibited no specific influence upgn the diabetic condition, but
can be recommended within proper limits for their beneficial effects
upon the general health and spirits of diabetic patients.

CHAPTER VI.

THE INFLUENCE OF FAT IN THE DIET.

Some references to the literature on this topic will be found in preced-
ing chapters. It suffices here to mention that the accepted doctrines
in practice have been as follows-: that fat is the most useful food in
diabetes; that it is responsible for little or no glycosuria; that its use
need not be restricted even from the standpoint of acidosis unless in
the presence of threatened coma, because deficiencies of fat in the diet
are made up by the use of body fat in metaboUsm; that diabetic
patients should be built up in weight if possible and their nutrition
maintained at a masdmimi by a full caloric ration, especially of fat, the
calories lost as sugar and acetone bodies in the urine being also replaced
by fat in the diet; and that undernutrition should be employed only
in the slight degree and brief duration recommended by Naunyn. In
opposition to these beliefs and this usage, the conclusion has been
reached, especially from animal experiments, that diabetes is a dis-
order of the total metabolism and that any increase of weight or of
total diet increases the strain upon the weakened function. Accord-
ing to this assumption, rational treatment would consist in first cutting
down the metabolic strain to a minimiun by fasting until active
S3mciptoms are controlled, and thereafter in permanently maintaining
a reduced level of weight and metabolism to correspond to the weak-
ened function. To some extent the question at issue is divisible
into the influence of body weight in itself and the influence of the diet
in itself. The various factors have been studied more particularly in
the animal experiments, but the same classification may conveniently
be employed for the observations on human patients, which are in all
respects confirmatory.

500

INFLtTENCE OF FAT IN THE DIET 501

A. Influence of Body Weight.

Since the weight (broadly speaking and without considering fluc-
tuations of water content of the body) necessarily rises and falls with
the supply of available calories, a sharp differentiation of the influence
of weight as distinct from the diet producing it is difficult. Three
Unes of evidence may be mentioned.

One of these consists in the marked benefit to the diabetes, the
clearing up of all active symptoms, and the striking gain in assimi-
lative power when the body weight is reduced. Examples are afforded
in the histories of patients Nos. 12, 16, 21, 33, 35, 41, 46, 57, and 60.

The second line of evidence consists in observations of the effect of
increase of weight. In the milder grades of diabetes such influence
may be less obvious, though still frequently demonstrable, but in the
moderate or severe grades of the disorder the influence is too plain
to be missed. In anything resembling a severe type of diabetes, the
present series has afforded no exception to the rule, which is be-
lieved to be general, that gain in weight means loss in tolerance.
At a suitable level of weight patients or animals may remain free
from diabetic symptoms for long or indefinite periods. If the diet,
especially by addition of fat, is made such that the weight increases,
symptoms may remain absent until some higher level of weight is
reached, differing according to the severity of the diabetes. At this
point active symptoms return, and continue unless checked by re-
duction of weight. Examples of this parallelism between body weight
and diabetic symptoms are pointed out in the histories of patients
Nos. 5, 16, 23, 26, 41, 57, and 66. In most of the other cases such a
parallelism is more or less clearly illustrated. The entire treatment
by which freedom from diabetic symptoms is maintained has for one
of its constant objects the maintenance of a suitably low weight.

A third line of evidence is furnished by exercise, by which the body
weight can be controlled to an important degree without variations
in diet. It was concluded in the previous chapter that exercise has no
apparent specific influence upon the essential diabetic disorder. This
being the case, it is instructive that the sugar in blood and urine and
other diabetic symptoms can to some extent be controlled by exercise
without change in the diet. Examples of the checking of undue rise

502 CHAPTER VI

of weight and corresponding control of diabetic symptoms by exercise
are shown in the histories of patients Nos. 23, 37, and 42. In no in-
stance was exercise carried out in such manner as wholly to prevent
gain in weight. To this extent the studies are not decisive, and
the failure of exercise here, in respect to merely delaying and not
ultimately preventing the return of active diabetes, may thus receive
at least a partial explanation.

B. Intltjence of the Total Diet.

Inasmuch as the harm of either carbohydrate or protein in excess
of the tolerance has long been recognized, this question pertains es-
pecially to the influence of fat feeding; and this is divisible into the
influence upon acidosis and the influence upon glycosuria. In some
of the following cases the diets were such as to increase the body
weight slightly. In other cases the increase in weight was trivial
or absent, so that the effects noted must be attributed directly to the
changes in diet.

The production of glycosuria, and also of acidosis as indicated qual-
itatively by the ferric chloride reactions, was shown in Table IV of the
preceding chapter. Similar injurious effects attributable predomi-
nantly to high fat rations were described in cases Nos. 1 and 17 and
more particularly in case No. 5 (Chapter III). The production of
acutely threatening acidosis by small quantities of fat and relief of
this acidosis by diminishing the fat intake were shown in the his-
tories of patients Nos. 54 and 60. Also reference may be made to the
history of patient No. 57, where tests showing the effect of fat in
diminishing carbohydrate tolerance are described.

The history and graphic chart of patient No. 24 show how the fre-
quent traces of glycosuria were stopped, and the high blood sugar
reduced to normal, by means of reduction of fa:t and total calories,
while protein was given in larger quantity than before. Also the
tolerance was markedly improved as the body weight diminished with
this undernutrition.

In addition to the liberal use of fat in ordinary diabetic diets, it has
been administered heretofore in large quantities on oatmeal days,
vegetable days, and even fast-days, in the belief that much available

INTLUENCE OF FAT IN THE DIET 503

energy was thus supplied without appreciably injuring the carbo-
hydrate tolerance or causing any important degree of acidosis. Ob-
servations early in the present series indicated the harmfulness of
such use of fat. For example, in the histories of patients Nos. 2
and 4, it was pointed out how the acidosis increased and glycosuria
was unduly persistent when olive oil was given in addition to green
vegetables, whereas in the same and other patients periods of green
vegetables alone have acted powerfully in aboHshing acidosis.
These results in case No. 2 are shown more clearly by Table I.

The comparison of the two fast-days, April 30 and May 7, when the
patient was free from glycosuria, gives the impression that both were
beneficial in diminishing acidosis, although 100 gni. oKve oil were
given on the former day. This result on April 30 is readily explain-
able by the fact that the fat and total calories were decidedly lower
on that day than on the preceding and following days. It is signifi-
cant that the ammonia on April 30 did not show such a fall as usually
results from a plain fast-day. Though the harmful effect of this
quantity of fat on a single day may seem negligible, the damage
becomes more evident when a series of days is compared.

Period I in Table I was made up of vegetable days with lib-
eral addition of fat. Glycosuria was present, and the increase of
acidosis is shown by both the ammonia and acetone excretion, not-
withstanding the rather high carbohydrate intake and strongly
positive carbohydrate balance.

In Period II the fat allowance was sharply diminished. The glyco-
suria already begun continued through this period, and the carbo-
hydrate balance was lower than on April 23 and 24, yet the fall in the
ammonia and acetone output is well marked.

In Period III, continuing the same protein and carbohydrate
ration, the fat (olive oil) was again increased, and on the second day
of this period the increase of both ammonia and acetone was
again well marked.

Period IV was characterized by a diminishing fat ration and a
practically carbohydrate-free diet up to May 6. The diminution in
ammonia and acetone ran parallel to the reduction of fat, and the
sudden addition of 54 gm. carbohydrate onMay6 did not appreciably
increase the rate of fall of the acidosis.

504

CHAPTER VI

TABLE I.
Patient No. 2.

Diet.

Weight.

Urine.

Date.

Protein.

Fat.

Carbo-
hydrate.

Calor-
ies.

Volume.

Sugar.

NHs-N

Acetone
bodies
(as/S-

oxybu-
tyric).

Periods.

IDU

gm.

gm.

gm.

kg.

cc.

gm.

gm.

gm.

Apr. 21

Fast-day.

42.2

685

0.48

0.47

1.97

I

" 22

8.1

201.7

24.2

2008

41.9

1165

0

0.97

1.82

" 23

32.6

186.0

89.3

2137

41.8

1192

+

1.06

4.21

" 24

40.7

201.9

95.0

2432

42.2

1068

1.92

1.83

5.56

Apr. 25

38.9

57.9

74.2

1001

42.8

735

0.74

1.06

1.54

II

" 26

25.8

5.4

74.3

459

42.4

1970

3.15

0.50

1.62

" 27

25.8

5.4

74.3

459

42.2

2180

+

0.44

1.66

Apr. 28

25.8

155.4

74.3

1854

41.8

745

+

0.31

0.83

III

" 29

25.8

155.4

74.3

1854

42.1

1810

0

1.18

3.01

Apr. 30

—

100.0

—

930

42.1

1280

0

1.04

0.65

May 1

29.5

141.5

1.0

1440

41.2

990

0

1.12

2.22

IV

" 2

30.6

142.1

1.0

1450

41.8

1510

0

1.66

2.96

" 3

30.6

102.0

1.1

1077

41.6

930

0

1.35

0.85

'

" 4

26.2

99.9

1.0

1040

42.0

1530

0

1.19

0.85

" 5

29.2

76.4

1.0

985

41.6

1285

0

1.00

0.57

" 6

36.8

78.0

54.0

1096

41.7

1535

0

0.80

0.61

May 7

Fast-day.

41.6

1230

0

0.43

0.41

May 8

32.7

67.0

83.0

1097

41.0

1830

0

0.44

0.49

V

« 9

33.1

66.4

76.4

1076

41.3

2080

0

0.24

0.33

" 10

39.1

65.8

80.8

1062

41.2

1670

0

0.48

0.14

" 11

Fast-day.

41.3

1820

0

0.53

0.34

" 12

26.4

44.0

86.7

872

39.7

1140

0

0.19

0.27

" 13

32.4

39.8

104.0

928

40.4

2080

0

0.52

0.49

" 14

29.5

40.0

93.2

875

40.7

2157

0

0.32

0.49

" IS

44.8

45.3

140.6

1180

40.2

2205

0

0.35

0.32

Period V was another vegetable period with much less fat than in
Period I. The ammonia and acetone excretion was consistently low,
and though the protein ration was about the same and the carbo-
hydrate somewhat higher than in Period I, glycosuria remained
absent. The steady undernutrition which had reduced body weight
by 2 kilograms doubtless contributed to the acquisition of this
increased tolerance.

INFLUENCE OF FAT IN THE DIET SOS

The observations on this same patient in June and July, 1914, were
also instructive concerning the practical use of fat, especially for the
famihar purpose of building up the weight of diabetic patients. The
use of carbohydrate and the maintenance of as favorable a carbohy-
drate balance as possible has often been recommended as the most
important means of combating the resulting acidosis. The following
observations on this patient exemplify the failure of such a poKcy.

Here the body weight was increased by over 3 kilograms up to
June 30, essentially by the addition of fat. Table II shows how
acidosis ran parallel to the fat intake. The influence of the fat ration
in producing glycosuria also is suggested by this study and proved
by those mentioned later in this chapter. Carbohydrate was not
the sole cause of glycosuria, because, for example, it was higher
in Periods I and III on -days without glycosuria than in Period V
with marked glycosuria. Protein is not excluded as a factor in the
production of the glycosuria. The particular point, however, is the
manner in which the carbohydrate balance was successfully main-
tained and even increased during the periods of glycosuria and
acidosis. It will be observed that acidosis was increased with a high
positive carbohydrate balance in Period IV when the fat ration was
high, and diminished with a lower carbohydrate balance in Periods
III, VI, and the first part of VII, when the fat ration was low. Also a
more liberal protein ration did not serve to prevent acidosis in the
high fat periods. The study thus affords an example of the
general rule that the acidosis resulting from the attempt to build up
strength and weight by addition of fat to the diet is not prevented
by an increased utilization of protein and carbohydrate, but that this
acidosis falls when the fat intake is reduced. In Periods VI and VII
the injury from the high fat ration was thus relieved by diminished fat.
The body weight was likewise diminished. A glance at the graphic
chart (Chapter III) will show that this patient then (July and
August, 1914) was able to maintain herself at this reduced weight on a
well balanced mixed diet with the requisite restriction of total calories.

The respective parts played by protein and fat in producing glyco-
suria are illustrated in Table III.

In Period I, with the protein intake constant at 40 gm., the total
calories were gradually increased by addition of fat. The table shows

506

CHAPTER VI

n

tvi

1

Period I.
Low calory diet; high carbohydrate.

Total :calories for 5 days 5555; avKrage per day 1111.
Protein " 5 " 315.7 gm. " " " 63.1 gm.
Fat " 5 " 243.6 " " " " 48.7 "
Carbohydrate " 5 " 486.6 " " " " 97.3 "
Sugar excreted " 5 " 2.0+ " " " " 0.4 "
Ammonia nitrogen " 5 " 2.72 " " " " 0.54 "
Acetone bodies "5 " 2.33 " " " " 0.46 "

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INFLUENCE OF FAT IN THE DIET

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508

CHAPTER VI

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INFLUENCE OF FAT IN THE DIET 509

the resulting glycosuria, hyperglycemia, and increase of ammonia
excretion. The fast-day of October 18 diminished the ammonia
output as usual. In the next two periods the ammonia and blood
sugar are unfortunately deficient.

It is seen, however, that in Period II the total calories were kept con-
stant at the low level of 800, while protein was increased by 5 gm.
daily. The severity of the diabetes was such that glycosuria was
thus readily produced. It is also evident that small quantities of pro-
tein produced glycosuria more promptly and strikingly than consid-
erably larger quantities of fat, in keeping with the behef that protein
is a direct sugar-former.

In Period III the protein was constant at 50 gm., i.e. 10 gm.
higher than in Period I, and the fat was again gradually increased.
With the higher protein intake it is seen that glycosuria appeared at a
lower level of total calories than in Period I. Though the quantities
of sugar excreted were trivial, the increased protein allowance did not
prevent the development of distinct ferric chloride reactions at the
close of Periods II and III.

The following three observations show the effect of changes in the
fat intake, particularly upon the carbohydrate tolerance. Table IV
(compare also graphic chart. Chapter III) shows how, with a con-
stant diet of protein and carbohydrate, increase of fat through suc-
cessive weeks increased the body weight, but at the same time gave
rise to both sugar and ferric chloride reactions in the urine. On
carbohydrate-free diet, with the same protein and greatly reduced
fat, not only glycosuria but also acidosis was absent for 6 weeks there-
after. As evidences of acidosis, in addition to the ferric chloride
reactions, the graphic chart shows that the ammonia was slightly
lower and the plasma bicarbonate slightly higher, on the carbohy-
drate-free diet with reduced fat. On this diet the patient at a reduced
weight was able to remain free from diabetic symptoms.

Table V (see also graphic chart, Chapter III) shows how a pa-
tient was able to tolerate a diet with 10 gm. carbohydrate in the
week November 1 to 6. In the following weeks, without change in
protein, the fat intake was increased, and traces of glycosuria devel-
oped accordingly. Slight sugar and ferric chloride reactions then per-
sisted as the fat was further increased, notwithstanding the omission

510

CHAPTER VI

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m .4J

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53 .-^ 53

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CM H 111 (K f

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T3

INFLUENCE OF FAT IN THE DIET

511

Period II.
Protein fat diet, increasing protein, calories remaining

constant.
Total calories for 6 days 4804; average per day 800.
Protein increasing from 40 to 65 gm.
Fat for 6 days 378.4 gm., average per day 63 gm.

1

1
s

Period III.
Protein fat diet, protein constant, fat increasing.
Total calories for 6 days 5857.
Protein for 6 days 300 gm., average per day 50

gm.
Fat for 6 days 385 gm., increasing from 53.5 to

69.5 gm.

64.1

0.202

O O O O O J.

o

O O O O O _J.

1.44
1.23

1

1 1 M 1 1

oo . + + +

+ + + +

+

00+0+ +

t-i ■.-H -^ o\ r* (N

■g g g s s g

so

o
in

t~- •* » lO o ^o
1:^ (N f^ CN CN CN

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M I'M 1

lO lO LC 0\ CO t^

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\o vo \o VO lO lo

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S? £^ S S S S

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to »o »o lO »o »o

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-H C-) ts CS CM cs

i

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CS r4 CM cs f^ ro

+J ., .. ^ ., ..

0== - -- -

512

CHAPTER VI

TABLE IV.
Patient No. 26.

Diet.

Urine.

Blood.

Date.

Pro-
tein.

Fat.

Cai>
bohy-
drate.

Total
calories.

Sugar.

Feci,
reac-
tion.

Plasma
sugar.

Plasma
CO..

1

1915-16

em.

em.

gm.

em.

cent

ml. t"
cent

ie.

Oct. 25

0.135

52.5

27.5

" 26

0.263

56.0

" 25-31

304

664

85

7808

0

0

Average per day.

43

95

12

1115

27.8

Nov. 1

0.110

46.4

27.4

" 4

0.164

54.5

" 6

0.200

52.2

« i_7

330

979

90

10813

0

0

Average per day.

47

139

13

1544

27.1

Nov. 8

0.185

50.2

27.5

" 11

—

53.2

" 13

0.169

52.2

" 8-14

330

979

90

10813

0

0

Average per day.

47

139

13

1544

29.1

Nov. IS

0.100

49.2

28.2

" 18

0.167

—

" 20

0.185

45.9

" 15-2

330

1110

90

12022

0

+

Average per day.

47

160

13

1717

29.5

Nov. 22

0.113

40.9

28.0

" 24

0.189

50.8

" 27

0.232

48.5

" 22-2

330

1236

90

13190

0

++

Average per day.

47

176

13

1885

29.0

Nov. 29

0.154

53.2

28.7

Dec. 2

0.232

49.6

" 4

0.294

51.9

Nov. 29-Dec. 5

330

1346

90

14418

+++

++

Average per day.

47

192

13

2059

29.5

Dec. 6

0.107

58.6

28.6

" 9

0.316

58.6

" 11

0.303

53.7

" 6-13

346

746

78

8672

+++

++

Average per day.

43

94

9

1084

29.4

INFLUENCE OF FAT IN THE DIET

513

TABLE IV — Concliided.

Diet.

Urine.

Blood.

Date.

Pro-
tein.

Fat.

Car-
boliy-
drate.

Total
calories.

Sugar.

FeCla
reac-
tion.

Plasma
sugar.

Plasma
COj.

i

I91S-16
Dec. 14

" 14r-19

Average per day.

gm.

280
40

sm.

472
67

em-

5534
790

sm.
0

0

per
cent

0.156

ml. per
cent

51.8

kg.

29.7
30.2

Dec. 20-26
Average per day.

369

52

484
69

—

6007
858

0

0

-

-

29.1
29.5

Dec. 30

" 27-Jan. 2
Average per day.

360

51

486
69

5988
855

0

0

0.071

53.5

28.8
29.7

Jan. 5
" 3-9

Average per day.

360
51

390

55

—

5100
730

0

0

0.141

53.3

28.8
29.0

Jan. IS

" 10-16
Average per day.

360
51

390

55

—

5100
730

0

0

0.123

53.2

28.9
29.0

Jan. 17-23
Average per day.

360
51

390

55

—

5100
730

0

0

—

—

28.6
28.7

of all carbohydrate from the diet after November 24. With diminu-
tion of fat to make a total ration of 2000 calories, sugar and ferric
chloride reactions were entirely negative in the week December 6 to
11. Exercise was carried on throughout this time, but does not
detract from the conclusions of the dietary experiment.

Table VI (see also graphic chart. Chapter III) shows the record of a
woman who had just completed a test with green vegetables indicating
a carbohydrate tolerance of 240 gm. She was then placed on carbo-
hydrate-free diet,' on which she was free from both glycosuria and
acidosis. The blood sugar, doubtless by reason of the large carbo-
hydrate intake just preceding, remained high on November 15 to 17,
and then diminished. Fat was rapidly increased while keeping protein
constant. Both hj^erglycemia and glycosuria resulted. Also acido-
sis was shown both by the marked ferric chloride reactions and by the

TABLE V.
Patient No. 2.

Diet.

Weight

Urine.

Blood.

Date.

Protein

Fat.

Carbo-
liydrate

Total
calories

Sugar.

FeCls
reac-
tion.

Plasma
sugar.

Plasma
COs.

1915

«m.

gm.

gm.

kg.

per cent

Ml.

per cent

Nov. 1

Ill

131

10

1710

38.6

0

*0

—

" 2

111

131

10

1710

39.2

0

0

0.222

59.7

" 3

111

131

10

1710

39.6

0

0

—

—

" 4

108

133

10

1718

39.5

0

0

—

—

" 5

108

133

10

1718

39.8

0

0

0.270

49.9

" 6

108

133

10

1718

40.0

0

0

0.250

57.0

" 7 ,

Fast-day.

40.2

0

0

—

—

Nov. 8

108

163

10

2000

40.0

0

0

0.356

58.6

" 9

108

163

10

2000

39.8

0

0

—

• —

" 10

108

163

10

2000

40.3

0

0

0.370

44.5

" 11

108

163

10

2000

40.1

0

0

0.278

52'. 5

" 12

108

163

10

2000

40.2

0

0

—

—

" 13

108

163

10

2000

40.2

0

0

0.208

52.5

" 14

108

184

10

2193

40.3

+

0

—

—

Nov. IS .

108

184

10

2193

39.7

0

0

0.217

56.6

" 16

108

184

10

2193

40.2

0

0

—

—

" 17

108

184

10

2193

40.4

0

0

—

51.4

" 18

108

184

10

2193

40.3

0

0

0.208

53.2

" 19

108

184

10

2193

40.3

0

0

—

—

" 20

108

184

10

2193

40.2

0

0

0.227

55.0

" 21

Fast-day.

40.2

+

.0

—

—

Nov. 22

108

216

10

2495

39.0

+

0

0.294

57.9

" 23

108

216

10

2495

39.6

++

0

—

—

" 24

104

223

—

2496

39.7

++

+

0.383

48.6

" 25

104

223

—

2496

40.3

—

—

—

—

" 26

104

223

—

2496

40.0

+

+

—

—

" 27

104

223

—

2496

40.5

++

+

0.278

56.4

" 28

Fast-day.

40.6

—

—

—

—

Nov. 29

104

223

—

2501

40.3

—

0.213

58.9

" 30

104

223

—

2501

40.4

—

—

Dec. 1

104

223

—

2501

40.5

+

+

—

—

" 2

104

223

—

2501

40.4

+

+

0.270

48.4

" 3

104

223

—

2501

40.7

+4-

+

—

—

" 4

104

223

—

2501

40.7

++

+

0.244

52.8

"5

Fast-day.

40.3

0

0

—

—

Dec. 6

104

169

—

1995

39.7

0

0

0.344

55.2

" 7

104

169

—

1995

41.3

0

0

" 8

104

169

—

1995

42.0

0

0

" 9

104

169

—

1995

41.0

0

0

0.250

58.8

" 10

104

169

—

1995

40.8

0

0

" 11

104

169

—

1995

41.4

0

0

0.227

56.6

" 12

Fast-day.

41.3

0

0

—

—

514

INFLUENCE OF FAT IN THE DIET

515

TABLE VI.
Patient No. 47.

Diet.

Weight.

Urine.

Blood plasma.

Date.

Protein.

Fat.

Carbo-
hydrate.

Total
calories.

Sugar.

FeCIs
reac-
tion.

Sugar.

CO!

1915

gm.

em.

em.

he.

Per cent

vol.
per cent

Nov. IS

100

170

—

1992

60.2

0

0

0.20

50.8

" 16

100

170

—

1992

61.1

0

0

" 17

100

224

—

2492

61.6

0

0

0.23

" 18

100

224

—

2492

61.9

0

0

" 19

100

278

—

2994

62.0

0

0

—

" 20

100

278

—

2994

62.5

0

+

0.18

55.1

" 21

Fast-day.

62.4

0

+

—

—

Total for week.

600

1344

—

18440

Nov. 22

100

331

—

3492

61.1

0

-1-

" 23

100

332

—

3498

62.0

0

+

—

" 24

100

386

—

3995

62.6

0

++

0.22

51.9

" 25

100

385

—

3991

62.6

0

++

—

—

" 26

100

386

—

3995

62.7

0

++

—

—

" 27

100

386

—

3995

62.6

+

+++

0.20

39.0

" 28

Fast-day.

62.6

+

+++

—

— .

Total for week.

600

2204

—

22966

Dec. 6

100

167

10

2001

61.8

+

++

0.11

60.0

" 7

100

166

10

2001

62.8

+

0

—

—

" 8

100

162

20

1997

62.8

0

0

—

—

« 9

100

1S8

20

1961

63.2

0

0

0.18

59.4

" 10

100

163

20

2005

63.3

0

0

—

—

" 11

100

163

20

2005

63.1

0

0

—

—

" 12

Fast-day.

63.2

0

0

Total for week.

600

978

100

11972

Dec. 13

100

163

20

2005

62.3

0

0

0.13

66.9

" 14

100

159

30

2007

63.0

0

0

—

—

" IS

100

154.

40

2002

63.7

0

0

—

—

" 16

100

148

50

1993

63.6

0

0

—

—

" 17

JOO

143

60

1999

63.8

0

0

. —

—

" 18

100

140

70

1998

63.7

0

0

—

—

" 19

Fast-day.

64.3

Total for week.

600

909

270

12004

Dec. 20

100

148

50

1990

61.9

0

0

—

—

" 21

100

148

SO

1990

62.7

0

0

0.11

—

516

CHAPTER VI

decided fall in plasma bicarbonate, which evidently would have been
serious except for being checked by fasting. After the injury from the
fat had been corrected by an undernutrition period, December 1 to
5, the patient within 2 weeks demonstrated the ability to tolerate as
much as 70 gm. carbohydrate with the same protein as before, with

TABLE VII.
Patient No. 74.

Diet.

Urine.

Date.

Protein.

Fat.

Calor-
ies.

Vol-
ume.

Nitro-
gen.

NHs-N

100 NHs-N

Total
acetone
bodies.

Sugar.

N

1917

gm.

em.

em.

cc.

em.

gm.

gm.

Feb. 13

50

43

600

141S

9.66

0.93

9.6

0.82

Negative.

" 14

SO

43

600

1160

9.08

0.90

9.9

0.64

it

" IS

SO

43

600

1470

10.14

1.00

9.9

0.43

tt

" 16

50

43

600

1770

.11.35

1.10

9.7

0.58

ft

" 17

50

43

600

1440

9.76

0.99

10.1

0.45

11

" 18

]

^ast-day.

1145

6.25

0.84

13.4

0.45

(t

" 19

50

150

1600

1875

8.77

1.46

16.6

4.61

t(

" 20

so

43

600

1480

6.64

1.14

17.2

0.70

It

Blood Findings February

19 to 21.

Date.

Time.

Sugar.

Total
acetone
bodies

per
100 cc.

Com-
bining
power
for CO2.

Macroscopic appearance
of plasma.

1917

per cent

mg.

vol.
per cent

Feb. 19

7:00 a.m. (fasting).

0.14

31.8

62

Clear.

11:30 " (after first fat meal).

0.14

28.0

60

Slightly cloudy.

4:30 p.m. (3 hrs. after second fat

meal).

0.15

38.9

47

Milky.

11:30 p.m.

0.17

50.0

48

Cloudy.

Feb. 20

7:00 a.m. (fasting).

0.16

35.9

57

Slightly cloudy.

" 21

7:00 "

0.15

29.0

62

Clear.

fat diminished so as to limit the total diet to 2000 calories. Not only
was the urine normal, but it is seen that the blood sugar also fell to
normal. Fat was therefore clearly responsible for glycosuria, hyper-
glycemia, and acidosis in this case.

The immediate effect of a single large addition of fat to an other-
wise fixed diet was studied in greater detail in patient No. 74. The

INFLUENCE OF FAT IN THE DIET 517

diet was one of undernutrition, with a negative nitrogen balance,
though the deficit appears unduly large in the table because no
allowance is made for the nitrogen of the soup which was taken in
fixed quantities daily. On February 19, 107 gm. fat were added,
divided between the morning and noon meals. Though the blood
was not analyzed for fat, a tendency to pathological lipemia seemed
indicated, for the plasma was unusually opaque during digestion
and some cloudiness persisted in that obtained at 7 a.m. the next
day. During the earUest period the total acetone in the plasma
was not increased. Only at 4:30 pi.m., 3 hours after the second fat
meal and 9 hours after the first one, was such an increase demon-
strated. At 11 :30 p.m., when the lipemia had markedly diminished,
the maximum ketonemia was encountered. By the following morn-
ing it had fallen to nearly the same level as before the fat addition.
The plasma bicarbonate ran strikingly parallel, falling as the acetone
bodies rose, and rising thereafter, as they fell. There was also a
well marked increase of acetone bodies, of ammonia nitrogen, and
of the ratio of ammonia to total nitrogen in the urine. Also, instead
of a sparing of protein, there was an increase of nitrogen excretion on
this day. No glycosuria occurred, and though the slight increase in
blood sugar may be significant here as elsewhere, there is no indi-
cation that sugar was actually formed from the fat.

The effect of a smaller and more gradual addition of fat was tested
as shown in Table VIII. Glycosuria being absent on an under-
nutrition diet of 40 gm. protein and 500 calories, the fat tolerance was
tested by the addition of 5 gm. fat daily to this diet. Under the low
diet it is seen that the blood sugar diminished up to October 18,
whereas the fall in the acetone bodies was maintained only to Octo-
ber 16. Both then progressively increased, and excretion of both
sugar and acetone bodies in the urine developed correspondingly.
The rise of weight must be attributed chiefly to water retention, since
even with the low metabolism of this emaciated condition, genuine
gain in tissue is scarcely possible on the diets shown. The test indi-
cated a very low total food tolerance in this patient and the necessity
for extreme undernutrition if active symptoms were to be prevented.

A test of the sudden giving and withdrawal of a considerable
quantity of fat was made upon patient No. 75, as shown in

518

CHAPTER VI

Table IX and in the graphic chart (Chapter III) . By consulting the
graphic chart it can be seen that this patient had been kept in the
hospital from February 21, 1917, on diets up to 60 gm. protein and
1850 calories, with urine very comnaonly showing the faintest detec-
table traces of sugar and ferric chloride reactions, but never titra-
table quantities of sugar in the two month period. In correspond-
ence with the urine, the blood showed continuous hyperglycemia

TABLE vm.
Patient No. 69.

Diet.

Weight.

Urine.

Blood.

Date.

Protein.

Fat.

Alcohol.

Calor-
ies.

Volume.

Sugar.

Total
acetone
bodies
(as ace-
tone).

Sugar.

Total
acetone
bodies

in
plasma
(as ace-
tone)
peiiOO

cc.

19i6

gm.

em.

gm.

kg.

cc.

gm.

gm.

per cent

««.

Oct. 13

40

17

25

500

37.0

3850

0

0.51

0.20

26.6

" 14

40

22

25

546

37.4

2790

0

—

—

—

" IS

40

28

25

602

37.2

3170

0

0.49

—

—

" 16

40

33

25

649

37.1

2335

0

0.32

0.15

19.7

" 17

40

40

25

704

38.2

2370

0

0.36

—

—

" 18

40

45

25

750

38.0

2950

0

0.39

0.13

24.3

" 19 .

40

50

25

800

37.9

2515

0

0.41

—

—

" 20

40

55

25

855

38.0

2220

0

0.36

—

—

" 21

40

60

25

902

38.2

2755

0

0.61

0.14

33.4

" 22

40

65

25

958

38.9

2900

0

0.95

—

—

" 23

40

70

25

1005

38.0

3390

0

1.09

—

—

" 24

40

75

25

1051

38.0

3090

0

0.99

0.16

35.6

" 25

40

80

25

1107

38.6

2760

-t-

1.27

—

—

" 26

40

85

25

1153

39.0

2230

++

0.98

—

—

" 27

40

90

25

1205

40.8

6180

9.84

2.53

0.27

42.3

and a moderate increase of total acetone (31 mg. per 100 cc.) at the
time the test was made. A week before this (April 30) the protein
had been increased by 10 gm., and the diet at the beginning of the
test consisted of 70 gm. protein and 1500 calories. In addition
there was an allowance of 600 cc. clear soup and 800 gm. thrice
cooked vegetables daily, which were ignored in reckoning food values.
With the increase in protein, sugar reactions became slightly more pro-

TABLE IX.

Patient No. 75.

Diet.

Urine.

Blood Plasma.

(U

1.

,

la

Date.

H

-1

-i

Remarks.

4

-1

■3

■S

i,

i

S8

ill

o

1^

em.

8
cc.

o

3

•g
^

1

to

1^

w

8

|..

1917

em.

em.

kg.

cc.

gm.

em.

per
cent

vol.
per
cent

me.

May 7

70

131

—

—

1500

36.2

2615

0

+

—

—

—

" 8

70

131

—

—

1500

37.6

2370

0

+

—

—

—

" 9

70

131

—

—

1500

37.2

3080

0

+

—

—

—

" 10

70

131

—

—

1500

37.1

3440

+

+

—

—

—

" 11

70

131

—

—

1500

37.3

2860

0

0

—

—

—

" 12

70

131

—

—

1500

36,6

2440

0

+

—

—

—

" 13

Fa

ist-day.

37.2

3100

0

0

—

—

—

" 14

70

131

—

—

1500

36.2

2000

+

2.62

—

—

—

" IS

70

131

—

—

1500

37.4

2582

0

5.73

0.208

72.0

31.0

" 16

70

131

—

—

1500

37.5

2770

+

12.41

—

-^

—

" 17

70

131

—

—

1500

37.8

3142

++

17.58

—

—

—

" 18

70

131

—

—

1500

38.0

3340

++

5.98

—

—

—

" 19

70

131

—

—

1500

37.9

3152

++

3.18

—

—

—

" 20

Fe

ist-day.

37.2

2800

+

1.08

0.179

71.1

31.0

" 21

70

231

—

—

2430

35.8

2413

+

5.70

0.246

—

34.7

" 22

70

281

—

—

2895

37.4

2800

5.88

18.54

—

—

—

" 23

70

281

—

—

2895

38.0

3480

10.26

17.32

—

—

—

" 24

70

281

—

—

2895

37.6

3340

13.86

13.70

. —

—

—

« 25

70

281

—

—

2895

37.6

3630

16.29

18.65

—

—

—

" 26

70

281

—

—

2895

37.2

3435

18.87

15.98

0.200

47.1

83.0

5:00 p.m.

" 27

100

—

930

37.2

3377

18.54

7.61

0.238

57.6

63.5

10:00 a.m.

" 28*

70

281

—

—

2895

36.4

1955

7.40

18.10

0.263
0.208

69.1
63.5

71.3
89.2

9:00 "
6:00 p.m.

" 29*

70

281

—

-^—

2895

37.5

3483

26.13

25.01

—

—

—

" 30*

70

281

—

—

2895

38.0

3448

22.87

49.73

0.216

57.8

108.0

5:00 "

" 31

70

11

—

__

391

38.2

3105

21.56

17.68

0.286

59.7

57.2

9:00 a.m.

June 1

70

11

—

—

391

37.9

•2520

22.32

4.24

—

—

—

" 2

70

11

—

—

391

38.3

2728

18.83

1.85

—

—

—

" 3

Fe

ist-day.

38.5

2155

8.36

0.67

0.303

69.2

12,6

10:00 "

" 4

ti

38.2

2810

+

0.90

0.204

63.6

35.8

10:00 "

" 5

70

—

—

391

38.4

1760

+

0.81

—

—

—

" 6

70

—

—

391

39.2

3052

+

0.81

—

—

—

" 7

70

—

—

391

38.7

3030

+

0.33

—

—

—

" 8

70

—

—

391

38.8

3000

+

0.18

—

—

—

" 9

70

—

—

391

38.5

2790

+

0.50

—

—

—

" 10

Fast-

day.

—

38.6

3260

0

0.19

0.170 56.0

12.2

10:30 a.m.

* 20 gm. sodium bicarbonate on this day.

519

520

CHAPTER VI

TABLE IX — Concluded.

te.

Diet.

^

Urine.

Blood plasma.

Da

d

1

1

1

o

•3
u

■o

>

i

1

Is

8

Remarks.

1917

sm.

em.

gm.

cc.

kg.

CC.

em.

gm.

per
cent

wl.
per
cent

me.

June

11

70

11

—

—

391

38.1

2215

+

0.48

0.161

61.7

18.6

9:00 a.m.

cc

12

70

11

—

—

391

38.8

2050

+

0.18

—

—

—

a

13

70

11

—

—

391

39.9

3640

+

0.11

—

—

—

a

14

70

11

—

—

391

39.7

3830

0

0.11

—

— ■

—

u

15

70

11

—

391

39.3

3470

0

0.52

—

—

—

it

16

70

11

—

—

391

39.0

3435

0

—

0.164

—

8.3

5:00 p.m.

ti

17

Fast-c

ay.

39.0

4110

0

—

0.182

67.3

—

11:00 a.m.

((

18

70

—

70

881

38.5

1728

0

0.13

0.141

61.7

13.0

9:00 "

tt

19

70

—

70

881

39.9

3630

0

0.18

—

—

—

ti

20

70

—

70

881

39.8

3585

0

0.32

—

—

ti

21

70

—

70

881

39.4

3690

0

0.33

—

__

tt

22

70

—

70

881

39.0

2210

0

—

—

—

—

It

23

70

—

70

881

38.6

3060

0

—

—

—

—

tt

24

Fast-da

y

100

700

39.0

4166

0

—

0.098

57.0

7.2

10:00 a.m.

tt

25

70

11

—

100

1091

38.4

2104

0

0.23

0.066

72.1

19.1

9:00 "

tt

26

70

11

—

100

1091

39.2

3340

0

0.23

—

—

—

it

27

70

11

—

100

1091

38.4

3555

0

—

—

—

—

It

28

70

11

—

100

1091

38.4

2975

0

—

—

—

—

tt

29

70

11

—

100

1091

38.6

3468

0

—

—

—

tt

30

70

11

—

100

1091

38.6

3685

0

—

0.12

55.1

11.1

5:00 p.m.

July

1

HI

—

3.6

100

721

39.0

4030

0

—

0.11

—

10:00 a.m.

(t

2

77

16.5

—

100

1170

37.6

1620

0

—

0.13

64.5

—

9:00 "

It

3

77

16.5

—

100

1170

39.4

3535

0

—

—

—

—

u

4

85

22

—

100

1250

39.0

3640

0

—

—

ti

5

85

22

100

1250

38.2

3230

0

—

—

tt

6

85

22

100

1250

38.2

2882

0

—

—

It

7

85

22

—

100

1250

38.0

3990

0

—

—

^'

it

8

111

—

3.6

100

721

37.8

3505

0

—

—

ti

9

85

22

—

100

1250

37.4

2678

0

—

—

ti

10

85

22

—

100

1250

37.2

4807

0

ti

11

95

22

—

100

1297

36.5

4225

0

ti

12

95

22

—

100

1297

36.3

2430

0

tt

13

95

22

—

100

1297

37.8

3015

0

tt

14

95

22

—

100

1297

37.5

2998

0

tt

15

—

100

700

38.0

3350

0

—

—

—

—

INFLUENCE OF FAT IN THE DIET 521

nounced in the urine, but no titratable quantity was excreted. Under
these conditions 100 gm. fat were added to the diet on May 21 and
another 50 gm. on May 22, so that the diet May 22 to 30 consisted
of 70 gm. protein, 281 gm. fat, and 2895 calories. Also 100 gm.
olive oil were given on the fast-day of May 27. The result, as seen
in the table and the graphic chart, was a prompt glycosuria and keto-
nuria of considerable degree, also a rise of sugar and still more marked
rise of acetone bodies in the blood, with a tendency to a lowering of the
bicarbonate reserve. Notwithstanding the giving of 100 gm. olive
oil on May 27, this fast-day accomplished part of the usual purpose.
There was no reduction of blood sugar. The blood taken at 10 a.m.
on May 27, before the oil had been given, showed benefit of absti-
nence up to that point in a lowering of total acetone and a rise in the
CO2 capacity. The 100 gm. oil were then given, and as this was so
much less than the fat of the regular diet, this day of undernutrition
apparently accomplished part of the benefit of a fast-day in checking
the rise of acetone and fall of CO2 capacity. The giving of 20 gm.
sodium bicarbonate on May 28, 29, and 30 lowered the blood sugar
only transiently if at all. It evidently safeguarded the plasma bicar-
bonate, but either failed to prevent the marked increase in plasma ace-
tone, or possibly contributed directly to this increase. On May 30
the total acetone had reached the dangerous level of 108 mg. per 100
cc, and the patient's clinical condition was so unfavorable that
prudence demanded a change in the diet. There was none of the
dyspnea characteristic of acid poisoning, but intoxication was mani-
fested by dizziness, malaise, weakness, and drowsiness. Beginning
May 31, fat was excluded from the diet as far as convenient, keeping
the protein ration unchanged. The table shows how in the remaining
3 days of that week all symptoms except the hyperglycemia strikingly
improved. The clinical transformation was equally plain. Traces of
glycosuria persisted up to June 13. Beginning June 18, the very
low ration was augmented by first 70 gm. and then 100 gm. alcohol,
but the total calories never exceeded 1300. Under this program,
not only was there cessation of glycosuria and of ketonuria (aside
from the trace indicated by a slight nitroprusside reaction), but also
by July 1 the blood was normal in sugar, acetone, and alkali reserve.
As an additional test of the relative importance of protein in produc-

522 CHAPTER VI

ing the former glycosuria, a gradual increase of protein was then
made, and it was found that with as much as 95 gm. protein and
1300 calories glycosuria was still absent on July 14.

Tests with both gradual and sudden addition of fat were performed
upon patient No. 43, as shown in Tables X and XI and in the
graphic chart (Chapter III) . This young woman entered the hospital
for her fourth admission on December 2, 1916, with heavy glyco-
suria and ketonuria. The condition was controlled by fasting and
low carbohydrate-free diet as shown in the graphic chart. Traces
of sugar at first persisted, but with continuance of undernutrition
sugar and ferric chloride reactions were negative after December 17,
on a diet of 50 gm. protein and 500 calories. Also 300 cc. clear
soup and 300 gm. thrice boiled vegetables were given daily and not
reckoned in the tables. At this point the test began with a
gradual regular addition of fat to the diet through successive weeks.
The diet in these earher weeks remained one of undernutrition.
H3^erglycemia was still present at the beginning of the test,
but with continued low diet up to January 7 a progressive fall can
be seen. Although the small additions of fat had little definite in-
fluence upon the acetone bodies in the blood, there was nevertheless a
distinct increase of the excretion in the urine. In general the im-
pression gained from this period up to January 7 is that fat gives
rise directly to acetone bodies, but does not directly give rise to sugar
in the body. As the diet continued to increase, the blood sugar rose
after January 7, not to an excessive height at any time, but enough
to make continuous hyperglycemia and thus to sacrifice the benefit
of the previous undernutrition. Also traces of glycosuria appeared
and became continuous. The acetone bodies reached their highest
point in the blood plasma with 76 mg. per 100 cc. on January 13
and 19. The rise in the blood was not progressive, apparently be-
cause the kidneys acted efficiently in removing the excess, so that the
urine showed a steady increase of acetone bodies in parallel with the
increased fat ration. The ammonia nitrogen showed a correspond-
ing gradual increase. The lowering of the plasma bicarbonate to 56
per cent on February 20 may or may not be significant. Though the
diet finally reached a high level for a patient of this size at rest,
weight was not gained, though there was probably a gam in body fat.

TABLE X.
Patient No. 43.

Diet.

Weight.

Urine.

Blood.

Date.

Pro-
tein.

gm.

Fat.

Calo
ries.

Volume.

Su-
gar.

NHs-N

Total
acetone

bodies

as

acetone.

Sugar.

Total
acetone
bodies

in
plasma
fas ace-
tone)
per 100
cc.

Plasma
COa.

191(

gm.

kg.

cc.

gm.

gm.

gm.

per cent

mg.

ml.
per cent

Dec. 18

50

32

500

34.0

2435

0

0.55

—

" 19

SO

42

595

34.0

2249

0

0.66

—

" 20

SO

S3

700

33.9

2485

0

0.95

0.49

0.27

25.2

59.0

" 21

SO

64

800

33.8

3080

0

0.92

0.46

" 22

50

64

800

33.6

2783

0

0.66

0.44

" 23

50

64

800'

33.7

3085

0

0.59

0.55

« 24

Fast-day.

33.8

1780

0

0.46

0.39

" 25

SO

64

800

33.4

2660

0

0.S9

0.72

" 26

SO

70

850

34.2

2770

0

0.65

0.80

0.21

26.2

60.0

" 27

SO

70

850

34.2

3350

0

0.78

0.62

« 28

SO

70

850

34.0

2820

0

0.62

0.48

" 29

SO

70

850

34.0

3235

0

0.67

0.55

" 30

SO

75

900

34.1

3980

0

0.80

0.48

" 31

Fast-day.

34.2

2350

0

0.61

0.31

1917

Jan. 1

SO

75

900

33.6

2515

0

0.63

0.70

0.2S

30.8

72.0

" 2

so

80

950

34.3

4855

0

0.82

1.26

" 3

SO

80

950

33.8

3750

0

0.76

0.94"

" 4

so

80

950

33.8

3790

0

0.77

0.68

" 5

so

80

950

34.3

4690

0

0.92

0.94

" 6

so

86

1000

34.1

3840

0

0.87

0.66

" 7

Fast-day.

33.9

2985

0

0.62

0.97

0.19

21.3

62.0

" 8

so

86

1000

33.5

3645

0

0.75

1.09

" 9

so

90

1050

33.5

4100

0

0.86

1.39

" 10

so

90

lOSO

33.4

3795

0

0.97

1.10

« 11

50

90

1050

33.5

3850

+

0.92

0.69

" 12
" 13

50

so

90
97

1050
1100

33.9
33.2

4175
3470

+
+

0.95
0.91

0.75
0.75

0.29

17.4

76.0

" 14
" IS

so

Fast-da
97

ly.
1100

33.3
33.1

2330

,3275

0
0

0.69
0.74

0.44
1.11

" 16

so

102

1150

33.5

4375

0

1.00

2.32

" 17

so

102

1150

33.4

4680

+

1.09

2.06

" 18
" 19

so
so

102
102

1150
1150

33.1
33.6

3810
3810

+
++

1.09
0.89

2.02
1.18

0.25

21.6

76.0

" 20

50

107

1200

33.8

4400

++

0.90

1.10

" 21
" 22

50

Fast-day.
107 1200

33.8

33.7

3980
2950

+

0

0.74
0.71

1.35
1.05

523

524

CHAPTER VI

TABLE X — Concluded.

Diet.

Weight.

Urine.

Blood.

Date:

Pro-
tein.

Fat.

Calo-
ries.

Volume.

Su-
gar.

NHa-N

Total
acetone
bodies.

Sugar.

Total
acetone
bodies

in
plasma
(as ace-
tone)
per 100
cc.

Plasma

1917

gm.

em.

kg.

cc.

gm.

gm.

em.

per cent

m«.

ml.
per cenl

Jan. 23

50

112

1250

33.9

4170

0

0.97

1.00

" 24

50

112

1250

33.8

4575

0

1.07

1.66

" 25

50

112

1250

33.9

4390

+

1.07

0.71

" 26

50

112

12S0

34.0

4035

++

0.99

0.89

0.27

22.2

69.0

" 27

SO

117

1300

34.0

4780

++

0.93

0.91

" 28

Fast-day.

34.2

3140

+

0.49

0.53

" 29

50

117

1300

33.4

2960

0

0.49

0.86

« 30

SO

122

1350

33.4

4425

0

0.81

1.64

" 31

50

122

1350

34.0

5325

+

0.94

2.77

Feb. 1

50

123

1350

34.0

3640

+

0.83

1.38

" 2

50

123

1350

34.0

4360

+

0.99

2.44

0.29

23.4

67.0

" 3

SO

128

1400

34.4

4690

+

0.99

1.59

« 4

Fast-day.

34.3

3330

+

0.67

1.67

" 5

50

128

1400

33.6

3175

0

0.84

1.37

" 6

50

134

1450

34.0

3800

0

0.82

1.75

0.35

24.8

61.0

" 7

SO

134

1450

34.0

4S9S

+

1.43

2.57

" 8

SO

134

1450

33.9

4490

+

1.21

2.83

" 9

50

134

1450

33.9

4690

+

1.12

2.86

" 10

50

139

1500

34.0

4380

+

1.00

3. 85

" 11

Fast-day.

34.0

1980

+

0.59

1.23

" 12

SO

139

1500

33.5

2905

+

0.72

1.60

" 13

SO

144

1550

33.6

4670

+

0.97

3.41

0.24

25.4

65. 0

" 14

50

144

1550

33.0

4650

+

1.09

2.65

" IS

50

144

1550

32.8

3955

+

1.08

2.14

" 16

SO

144

ISSO

32.5

3735

+

1.37

3.78

« 17

SO

ISO

1600

32.6

4000

+

1.16

2.88

" 18

Fast-day.

32.8

1370

+

0.76

0.60

" 19

50

150

1600

32.2

3420

+

0.97

3.32

" 20

SO

85

999

32.2

4820

+

1.40

0.26

29.25

56.0

" 21

50

85

999

32.4

3791

+

1.12

" 22

50

85

999

32.7

3988

+

0.90

« 23

SO

86

1002

32.7

4645

+

0.90

" 24

50

85

999

33.0

3750

+

0.77

0.27

52.0

" 25

Fast-day.

33.3

3190

+

0.53

" 26

SO

85

999

32.9

3228

0

0.42

« 27

SO

85

999

32.4

4040

0

0.57

0.23

« 28

60

81

1000

33.3

4767

0

0.68

INFLUENCE OF FAT IN THE DIET 525

masked by a loss of water driven out by the fat feeding. There was
no improvement in strength or comfort. As a whole, the test
indicated distinct injury to the patient from the laboratory stand-
point by the cautious addition of fat in excess of the assimilative
power, with no compensating clinical benefit.

Beginning February 20, the fat was reduced to make a total diet of
1000 calories. Glycosuria gradually cleared up and the ammonia
excretion diminished.

On February 28 the protein was increased to 60 gm., keeping the
total calories at 1000. Faint traces of glycosuria appeared on some
days thereafter (see graphic chart). On March 14 the fat was in-
creased to make 1100 total calories, arid again on April 18 to make
1300 calories. On April 23 the fat was further increased to make
1500 calories, but then diminished on May 2 to 1300 and on May 7
to 1200 calories. During this whole period of 2 months the patient
was obviously just at the edge of her tolerance, showing faint sugar
and ferric chloride reactions very frequently, but never excreting a
titratable quantity of sugar or developing any marked acidosis. In
the first week shown in Table XI (May 14 to 20) the condition made
an evident change for the worse, for on the identical diet as much as
11 gm. sugar and 2.3 gm. acetone bodies were excreted on certain
days. The opportunity seemed favorable for testing whether this
change represented "spontaneous downward progress" on the part
of the patient, or whether it was merely the culmination of several
months of diet slightly overtaxing the tolerance. A sudden addition
of 100 gm. fat was made on May 21, with an additional 50 gm. on
May 22, thus raising the total diet to 2600 calories. Marked and
continuous glycosuria and ketonuria followed, as shown in Table XI
and in the graphic chart. Also the total acetone increased in
the blood plasma, and the alkah reserve fell as low as 42.3 per cent
on May 26 and 27. The patient, who had welcomed the opportunity to
eat more, quickly became unwell and unhappy. The daily adminis-
tration of 20 gm. sodium bicarbonate on May 28, 29, and 30 seemingly
lowered the blood sugar and urine on the first day, but had doubtful
eifect thereafter. It also raised the plasma bicarbonate temporarily,
but by May 30 this was again down to 43.7 per cent in spite of the
alkali dosage. It is also possible that this dosage may have been

TABLE XI.
Patient No. 43.

Diet.

Urine.

Blood plasma.

Date.

1

1

1

•3

8

<

u

2
1

B

I

^

i

1

o
o

vol.
ter
cent

mg.

Remarks.

1917

gm.

gm.

gm.

cc.

kg.

cc.

gm.

gm.

pit
cent

May 14

60

103.0

—

—

1202

33.0

3510

0

1.49

—

—

— ■

" 15

60

103.0

—

—

1202

33.4

5070

+

2.30

0.192

55.7

49.0

" 16

60

103.0

—

—

1202

32.9

5075

5.04

1.71

—

—

—

" 17

60

103.0

—

—

1202

33.8

5215

10.90

1.61

—

—

—

" 18

60

103.0

—

—

1202

34.0

5200

10.40

2.24

—

—

—

" 19

60

103.0

—

—

1202

34.3

5640

10.90

1.28

—

—

—

" 20

Fast-day.

34.1

1895

7.22

1.03

0.213

64.5

21.8

" 21

60

203.0

—

—

2132

34.8

3330

+

2.10

0.175

—

29.8

" 22

60

253.0

—

—

2597

34.9

5720

+

7.01

—

—

—

" 23

60

253.0

—

—

2597

34.6

4740

18.01

9.48

—

—

—

" 24

60

253.0

—

—

2597

33.9

3205-1-

18.99

10.63

—

—

—

" 25

60

253.0

—

—

2597

34.2

2680

18.52

9.58

—

—

—

" 26

60

253.0

—

2597

34.2

2280

13.80

9.57

0.298

42.3

5: 00 p.m.

« 27

30.0

—

279

34.6

2035

35.60

9.80

0.233

42.3

—

10:00 a.m.

" 28*

60

253.0

—

2597

33.7

1090

5.67

8.61

0.286
0.154

57.6
48.3

52.1
77.5

9:00 "
6:00 p.m.

" 29*

60

253.0

—

—

2597

35.6

2995

24.06

18.41

—

—

—

" 30*

60

253.0

—

—

2597

34.4

3475

24.84

17.25

0.222

43.7

99.0

5:00 "

« 31

60

10.0

—

—

332

35.4

5115

45.72

11.18

0.216

48.3

52.1

9:00 a.m.

June 1

60

10.0

—

—

332

34.9

5645

31.90

4.46

—

—

—

" 2

60

10.0

—

—

332

35.0

4845

24.23

1.55

—

—

—

" 3

Fast -day.

—

35.5

1575

8.80

1.31

0.228

57.9

40.8

" 4

(C

—

34.8

860

+

1.29

0.170

58. 9

42.3

" 5

60

4.0

—

—

282

34.4

4100

+

2.01

—

—

—

" 6

60

4.0

—

—

282

34.6

4900

+

0.88

—

—

" 7

60

3.0

—

—

275

35.4

5440

+

0.49

—

—

« 8

60

3.0

—

—

275

34.9

3570

+

0.51

" 9

60

3.0

—

—

275

34,5

4520

+

0.36

_

" 10

Fast- day.

—

34.1

1855

+

0.31

0.208

64.5

43.1

10:00 a.m.

« 11

59

—

—

—

249

34.4

4005

+

0.64

0.159

59.8

20.4

9:00 "

" 12

59

—

—

—

249

34.4

4660

0

0.42

—

" 13

59

1.0

1.0

—

255

33.0

4610

0

0.41

—

« 14

59

1.0

1.0

—

255

33.4

4820

0

0.29

" IS

59

1.0

1.0

—

255

33.8

4605

0

0.23

" 16

59

1.0

1.0

—

255

34.2

5250

0

0.47

0.128

—

13.4

5:00 p.m.

" 17

Fast- day.

34.3

2230

0

0.54

0.200

67.3

—

11:00 a.m.

" 18

59 1.01.0 40

535

33.8

3640

0

0.18

0.113

—

26.6

9:00 «

* 20 gm. sodium bicarbonate on this day.

526

INFLUENCE OF FAT IN THE DIET 527

partly responsible for the maximum of 99 mg. total acetone per 100 cc.
of blood plasma on May 30. Here also dyspnea was not present, but
on account of general malaise the patient was glad to discontinue the
fat ration.

Accordingly on May 31 fat was eliminated from the diet as far as
convenient, keeping the protein unchanged. The first effect was seen
upon acidosis, in the fall of acetone bodies in blood and urine, the
spontaneous rise of the plasma bicarbonate, and the reHef of the
clinical symptoms. The sugar excretion rapidly diminished. The
hyperglycemia was more stubborn, but there was a progressive di-
minution down to a normal level on June 18, following the fast-day
of June 17. Thereafter it proved possible, as in the preceding pa-
tient, to increase the protein to 84 gm. daily without glycosuria. In
another test, not included here, a similar return of diabetic symptoms
followed an increase of the total calories of the diet.> The s3Tnptoms
were again abolished by diminution of calories without change in
protein. It has also been possible to prolong the freedom from active
symptoms up to the present, so that "spontaneous downward
progress," if existent, has not as yet been manifest.

This question of downward progress has been investigated by long
as well as short feeding experiments on animals, but it is seldom that
circumstances permit a similar close comparison between individual
human patients treated on opposed principles. It has come about
that without experimental intent, treatment was carried out along
opposite Unes in two patients of the present series, so closely com-
parable as to afford the most exact comparison possible in clinical
observations. These are patients Nos. 37 and 66. It will be seen
from their histories that both represented juvenile diabetes of the
usual type. Both cases were controlled by treatment in such man-
ner as to restore normal conditions in both urine and blood as far as
determined by the routine tests'. The condition of the two appeared
equally favorable from the clinical standpoint. The treatments dif-
fered in respect to the total calories of the diet. After the prelimi-
nary fasting and undernutrition which cleared up symptoms, the
boy (No. 37) was treated along former orthodox lines. He was
allowed a high caloric ration supposedly suitable for his age, with the
idea of facilitating normal growth and development. Exercise was

528 CHAPTER VI

employed to build up his muscles and consume surplus food. He was
discharged from the hospital with nearly the same body weight as
at entrance, and, with his feeling and appearance of splendid health,
seemed to afford an example of the most successful treatment. He
followed the diet with absolute fidelity and for a short time enjoyed a
practically normal existence. 2 months after leaving the hospital,
and 7| months from the onset of the diabetes, marked hyperglycemia
was found without glycosuria or other sjonptoms. This plain warn-
ing was met only by diminution of carbohydrate, not of the total
diet or weight. The blood sugar continued to rise, and at the second
admission traces of sugar and ferric chloride reactions were present
in the urine and the carbohydrate tolerance was found markedly re-
duced. The patient was allowed to go home after only 2 weeks in
the hospital, on a' diet of 40 calories per kilogram, at an increased
weight, with hyperglycemia continuously present. After this dis-
charge the progress was rather rapidly downward, and at the third
admission, 1 1 months after the first, the patient was almost in coma.
Much lower diets were then necessary, but the condition was still
never adequately controlled, especially as respects hyperglycemia.
After further steady downward progress, death occurred two years
after the first onset of diabetes. The result of treatment was favor-
able only to the extent that life and comfort had been so greatly pro-
longed, in a patient threatened with death within a few weeks or
months under other conditions.

The girl (No. 66) received such a diet in the hospital that she was
dismissed weighing 5 kilograms less than at admission. The two
patients were closely similar in natural size and weight. The boy had
been discharged on an average ration of 2100 calories, or 43 calories
per kilogram at his elevated weight. The girl was discharged on
an average ration of 1630 calories, or 3'6 calories per kilogram at her
reduced weight. This diet was slightly too high; for 5 months after
discharge, or 14 months after the onset of diabetes, blood samples
taken for observation purposes on 3 successive mornings before
breakfast showed a slight hyperglycemia of 0.130 per cent. This
warning was heeded by reducing the total calories to a little over
1300 average, by diminishing fat, while the protein was kept the
same, and the carbohydrate actually increased by 5 gm. Along

INFLUENCE OF FAT IN THE DIET 529

with the hyperglycemia there had been a gain of 8 kilograms in
weight. The reduced diet diminished the weight to 50 kilograms,
which was identical with that at the first admission. Both blood
and urine then remained normal. Later it happened that the girl
was placed temporarily on the same treatment as the boy; that is,
the fat intake was inadvertently increased, and the beginning of glyco-
suria was met by a reduction of 15 gm. carbohydrate in the diet.
Fortunately the increase of body weight aroused suspicion. On re-
calling the patient to the hospital, marked hyperglycemia and strong
acetone reactions were found. The mistake was corrected by reduc-
tion of fat and total calories, while the carbohydrate was again
increased by 15 gm. Accordingly, in contrast to the boy's death
2 years after the onset of diabetes, the girl still has the feeling and
appearance of perfect health, normal conditions in blood and urine,
and full possession of her original carbohydrate tolerance. She has
grown and developed normally, apart from being kept slightly but
not noticeably below maximum weight. The boy on his unduly
high diet developed glycosuria frequently with colds, but the girl
passed through an appendix attack without showing sugar. If there
is any "spontaneous downward progress" in her case, it has not yet
made itself manifest.

The only objection to the comparison must be based on the as-
siunption that the diabetes was inherently more severe and progres-
sive in the boy, and that the girl represented one of the unusual
juvenile cases with little progressive tendency. In support of this
assumption is the fact that the boy was close to coma within 3 weeks
from the onset of known symptoms, whereas the girl entered the
hospital without alarming symptoms, 5 months after the first sus-
picious signs of diabetes. The justice of the comparison is supported
by several considerations.

1. It has been the experience with this series of diabetic patients
that the most accurate measure of severity is found in the tolerance
for carbohydrate and other foods. Coma is often merely an incident
depending upon the character of the diet, and is not a reliable index
of the true assimilative function or progressive tendency. The girl
was 1 year younger than the boy and not so robust. The actual
fact is that during her several months of diabetes she had progressed

530 CHAPTER VI

downward to such an extent that her assimilation was distinctly
lower than that of the boy. In the initial test with green vegetables
the limit of her tolerance was 140 gm. carbohydrate, as compared
with 175 to 200 gm. for the boy. Furthermore, the capacity for
improvement was far more evident in the boy, for after 4j months
in the hospital he was able to tolerate 400 gm. carbohydrate, whereas
it can be seen from the girl's graphic chart that she showed glyco-
suria on May 18 and 29 on a slight increase of diet which was far
below the regular tolerance of the boy.

2. The progressive tendency in the girl's case was further demon-
strated by the hyperglycemia and other threatening signs on two dif-
ferent occasions when she happened to be subjected temporarily to
the same unfortunate kind of treatment as the boy. The harmful-
ness of an unduly high fat ration was thus proved also in her case.
The development of these sjonptoms more quickly and on a lower diet
than in the boy's case confirms the assimiption that the diabetes was
actually more severe in the girl.

3. The claim that the result in the boy's case was due solely to an
inherent progressive tendency could be supported only on the as-
sumption that he was somehow immune to the injurious effects of
high caloric diets. Such effects have been easily and plainly demon-
strable in every case tested, and the rule is believed to be without
exception for all typical cases of diabetes. In the light of the plain
evidence of all the preceding experiments, it can only be concluded
that the excessive caloric ration was one important cause of the
downward progress in the case of this boy. Downward progress has
thus far been avoided in the girl's case by avoiding such overstrain
of the metaboHc power. It is strongly suggested that a similar result
might have been obtained by similar methods in the boy's case, and
that his death within 2 years was not due to any inherent and in-
evitable process in himself, but directly to the lack of proper treatment.

Though experimental results place the principle of total caloric
restriction for diabetes on a basis not affected by the many variables
which determine cUni'dal success or failure, yet the general results of
treatment under this method, in comparison with the results obtained
with such fat diets as have heretofore been employed in the man-
agement of diabetes, constitute the most important body of evidence

INFLUENCE OF FAT IN THE DIET 531

in support of the practical usefulness of this plan. A number of case
histories in this series show the diasters which have occurred when-
ever the principle of total caloric regulation has been violated. On
the other hand, as far as the treatment has been properly carried out,
it is believed that the method of restricting fat and total calories in
the same manner as carbohydrate and protein has proved vaHd in its
conception and beneficial in its application.

CHAPTER VII.

RESULTS— PROGNOSIS.
Severity of the Cases.

A standard of severity of diabetes is difl&cult to define. In an at-
tempt to classify cases according to the actual degree of the diabetic
disturbance and the problems offered in treatment, the judgment of
severity has been formed from three factors, (1) carbohydrate toler-
ance, (2) age, and (3) clinical course.

1. Accepted criteria in the past have been the assimilation of car-
bohydrate added to a protein-fat diet, the intensity of glycosuria on
a given diet, acidosis, and (with a few authors) changes in protein
metaboUsm and the degree of difl&culty in bringing the urinary ni-
trogen quantitatively and quaUtatively to normal. If diabetes is a
disorder of the total metaboUsm, these indices based upon carbohy-
drate, fat, and protein metabolism are equally valid and yield equiva-
lent information. The essential thing is the power of assipiilating
food. Diabetes is severe in proportion as this power is deficient.
The choice of a test comes down to a question of convenience of per-
formance, ease and reliability of interpretation, and safety for the
patient. In some severe cases, the injury from excess of protein or
fat is promptly evident. Generally, however, the manifestation is
slower, and the injury is correspondingly more lasting. Carbohy-
drate acts most rapidly in producing glycosuria. Standard condi-
tions for comparison are provided by testing with carbohydrate alone
with exclusion of other foods. Glycosuria and hyperglycemia pro-
duced by pure carbohydrate subside promptly on its withdrawal, in
contrast to the slower rise and fall when they result from protein-fat
excess. Such a carbohydrate period, with its attendant undernu-
trition, acts favorably upon acidosis and upon the diabetes itself, so
that with intelHgent management a thetapeutic as well as a diag-
nostic purpose may be served. Diet and other accidental factors in-

532

RESULTS — ^PROGNOSIS 533

troduce many elements of confusion in the untreated case. When
the rush of symptoms is checked by fasting and perhaps a subse-
quent undernutrition period, until the acute condition is well con-
trolled, a carbohydrate test has ?,lways proved a reliable index of the
general food tolerance. Other conditions, such as noted below, being
equal, the food tolerance has afforded the best basis of judgment con-
cerning the existing grade of severity of the diabetes, comparisons be-
tween patients, and the degree of difl&culty to be anticipated in treat-
ment. A patient received in or near coma may have far milder
diabetes and be much easier to keep in good condition subsequently
than one received with slight or no active symptoms but with a mini-
mal assimilative power. Later tests give indications of the progress
when modifying influences are properly considered. For example,
with therapeutic reduction of weight there may be an apparent gain
of assimilation, and with increase of weight there may be an apparent
loss of assimilation, while the actual functional capacity is unchanged.
Increased tolerance at the same or higher body weight shows genuine
improvement.

2. Age is no absolute guide, for mild diabetes in children and severe
diabetes in the aged are known. In general, however, it is recognized
that the danger from diabetes is in inverse proportion to the age.
Two reasons may be assigned for the difference : first, the higher me-
tabolism in children especially imposes a heavier burden upon a weak-
ened assimilative function; second, the more severe type of diabetes,
occurring generally in the young, is a specific disorder of the islands
of Langerhans, seemingly partly functional in most cases, but subject
to rapid aggravation and organic degeneration of islands due directly
to overfeeding. The milder diabetes of later Hfe seems often or gen-
erally different in origin, perhaps from chronic rather than acute
pancreatitis; at any rate, it generally is less rapidly and seriously
affected by excesses of diet. The inherently milder form sometimes
occurs in children, and there is a possible hope that recovery from
both the pancreatitis and the diabetes may then be more complete
than in adults. It is useful to distinguish diabetes which is in a
mild incipient stage but is inherently and potentially severe. For
this reason every case of diabetes in a child calls for the most careful
treatmept from the earliest possible moment, preferably .under a

534 CHAPTER VII

specialist; and such juvenile diabetes, even in the early stage with high
tolerance, may be classified among severe cases, unless later experi-
ence proves it clearly to be of the rarer mild form. On the other
hand, no patient is so old that diabetes is harmless to him. No
senile diabetes is so free from progressive tendency as not to be ag-
gravated by prolonged diet keeping up active symptoms, or so mild
as not to carry the threat of gangrene, bhndness, or other form of
death or disability at any time. When, after experience with severe
cases ill young persons in this series, some older patients with long
standing diabetes were taken, the supposition that treatment would
be quick and easy proved to be a mistake. Not only are an appre-
ciable proportion of such patients subject to the danger of acidosis on
fasting, but their glycosuria may be very stubborn and hypergly-
cemia and acidosis still more so, the apparent food tolerance maybe
almost nothing, and months of rigorous undernutrition may be re-
quired if the condition is to be controlled. The patient and friends
may feel that a relatively harmless glycosuria has been exchanged
for a state of weakness and discomfort, for a merely theoretical bene-
fit expressed in the laboratory findings; but with perseverance in right
management, the reward is obtained in an evident improvement of
health, as well as in relief from lurking dangers. Notwithstanding
the necessity and the frequent difl&culty of rational treatment, the in-
fluence of age can generally be trusted to assist; laxness of methods
can often be tolerated to an extent which would be fatal in the
young. For example, when glycosuria is effectually controlled, the
stubborn hyperglycemia and slight ketonuria generally do not de-
mand the infliction of further acute privations upon the old person,
but will gradually diminish and disappear in the course of months,
provided always that the plan of diet is fundamentally correct. The
ultimate results as respects preservation of Kfe and the recovery of
strength and ability to take a satisfying diet are also, other things
being equal, generally more favorable in the old.

3. The clinical course of diabetes has always been an important
criterion of its severity. Until recently, the very acute cases in young
persons, terminating fatally within a few weeks, have stood as the
extreme type of severity defying all treatment. Fasting has proved
surprisingly successful in checking the progress of such cases, and it is

RESULTS — ^PROGNOSIS 535

established that they are often not the most severe as measured by the
food tolerance, and do not necessarily run the most rapid or unfavor-
able course. Nevertheless, the rapidity and degree of the break-
down of fat, carbohydrate, and protein metabolism, as shown by
acidosis, carbohydrate intolerance, high or "total" dextrose-nitrogen
ratios, and exaggerated protein catabohsm and aminosuria, must be
regarded as important evidence of the inherently dangerous and
progressive character of the case. Some allowance is necessary for
dietary, infectious, and other modifpng influences. For example,
an unwise protein-fat diet may bring on early coma. Likewise, in
cases Nos. 37 and 66, previously compared, the cold which marked
the onset of acute sjmaptoms in the former, and the larger appetite
of an athletic boy as compared with a delicate girl, might well be re-
sponsible for different rates of initial progress, without relation to
any differences in the specific diabetic condition. Sufficiently long
subsequent observation may prove that an occasional case, alarming
because of intensity of symptoms or its occurrence in a child or young
person, is actually mild or transitory in character. Diabetes dis-
covered with an acute infection is notably subject to this rule. For
example, among the pneumonia cases in the present series. No. 6
was presumably a mild diabetes rendered temporarily more severe by
the infection and resuming its chronic course thereafter; in No. 40,
either transitory diabetes was produced by the infection, or latent dia-
betes was made active and afterward became again latent. In aU
cases, the results of treatment are instructive. Patient No. 24 was
at an age when diabetes is generally more moderate in grade; his case
appeared severe, and the difficulty and slightness of improvement
with treatment gave the demonstration that it was actually severe. A
greater number of the elderly patients, as Nos. 12, 21, 33, and 35,
had diabetes which was severe from the standpoint of food tolerance
at the outset, but undernutrition finally revealed its essentially mild
or moderate nature. Obviously cases may progress from one stage
to another. If all the juvenile cases had been counted as severe at the
outset because of their youth, there would have been no place to
classify them after they had actually reached a worse stage. The
readiness with which progress occurs upward or downward may be
one index of severity. In the four cases last mentioned, it cannot be

536 CHAPTER VII

claimed that a change of type has been effected, at least up to the
present time, for if they regained their former weight they would
probably lose most of their apparent increase of assimilative power.
Examples of downward and upward progress are mentioned in the
review of cases below. The latter is notoriously more uncommon
and uncertain. Genuine changes of the grade of diabetes may be
considered as, representing, on the one hand functional deterioration
or anatomic degeneration, on the other hand functional recuperation
or organic regeneration of the islands of Langerhans. The abyss of
severity is found where the assimilative power is not only minimal,
but also rises little or not at all with the most thorough and prolonged
treatment.

Other occasional features carry some prognostic weight. One of
these is obesity. As noticed especially by the French cHnicians,
diabete gras is generally mild.^ But there is no sound basis for setting
this apart as a distinct tj^e, and plenty of cases of "fat" diabetes
carry a very bad prognosis unless the patients are reUeved of their
fat. The obesity in itself is always harmful, never beneficial or pro-
tective as so often supposed. The retention of an ordinary good state
of nutrition after years of diabetes is strong testimony for the essen-
tial mildness of the case, though rigorous and prolonged therapeutic
reduction of weight may prove necessary, and there is also the possi-
bility that the case may have turned rather rapidly severe toward
the close. The existence of or special susceptibility to any acute or
chronic infection is rightly classed among the gravest features in
prognosis, and the habitual immunity to infection displayed by many
diabetic patients, even on extreme undernutrition, is a strong point in
their favor. Such factors, however, properly belong among com-
plications, all of which have important influence upon the patient's
fate, but are scarcely elements of the diabetes itself.

Cases and Results by Decades.

Some statistical data are presented in the General Summary Table
of Chapter III. In the following survey, it has seemed useful to
adopt the well known plan of dividing the cases according to the dec-

^ The still better prognosis for fat diabetes with careful treatment is indicated
by the statistics of Hornor and Joshn, Am. J. Med. Sc, 1918, civ, 47-56.

EESULTS — PROGNOSIS 537

ades of life. An estimate of the severity is also given, on the com-
posite basis above outlined, chiefly upon the food tolerances, without
any absolute standard, since some arbitrary element is necessarily
involved in any such judgment.

The actual number of diabetic patients treated in this hospital to
date is 100, the total deaths 33, so that it would be possible, if desired,
to claim a mortality of approximately 30 per cent instead of the 43
per cent in the above table. A further reduction could be made by
subtracting five deaths (Nos. 11, 25, 34, 38, 46) not due to diabetes.
No. 48 was counted as dead because of the practical certainty of the
outcome under the circumstances. On the other hand, Nos.' 7 and
47 were counted among the living patients, though one was lost track
of and the other is near death from diabetes. The Hst of deaths will
probably be increased by Nos. 22, 58, and 61, from causes not chiefly
referable to diabetes.

The series was limited first to the cases received up to June, 1916, so
as to insure at least 16 months observation in every pubHshed case.
It was enlarged to include five fatal cases and three others (the severe
case No. 75 as the subject of special study, cases Nos. 73 and 76,
as examples of juvenile diabetes) from the number admitted since
that time. The omissions represent only a few mild cases and a
larger niunber of severe ones. These patients are known to be alive
and sugar-free, but have been observed for less than the specified
time. The selection of the list for pubHcation was governed by the
following considerations. First, some adequate period of observa-
tion is necessary for judging results in a chronic disease. Second,
the more recent cases present nothing different from the early stages
of the reported cases. Third, some of the cases were taken par-
ticularly for the study of acute acidosis. Some of them may be re-
ferred elsewhere for further treatment, and, if so, should be omitted
from our permanent statistics. Fourth, the purpose is merely to pre-
sent the most valuable 76 of the total 100 histories. Had a record of
high success been sought, it could easily have been obtained by slight
precautions in the selection of cases for treatment. For medical pur-
poses, failures are among the most instructive experiences; therefore
the pubHshed list was chosen to include all deaths, failures, and bad
results in the whole series, including those from discontinuance of
treatment, complications, or any other causes.

538

CHAPTER VII

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CHAPTER VII

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RESULTS — PROGNOSIS 541

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o o
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542

CHAPTER VII

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a »

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d

sift,- «§i 2 s&o-g sg.tS.ffi ° 'i >: t.,.ti-S

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544

CHAPTER VII

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Temporary control of -
symptoms on diets
too close to verge
of tolerance; aggra-

g
1

reatment.
nt on un-
ion; death
mo. after

diet.

benefit;
d prog-
ets slightly

ig toler-
ictions and
rrors con-

,

gi

Si's

tions of t

Improveme

demutrit

within 1

breaking

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downwar

ress on di

overtaxin
ance; infe
dietary e
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RESULTS — ^PROGNOSIS

545

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546

CHAPTER VII

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RESULTS — ^PROGNOSIS

547

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■go

3

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a

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2 .2
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548

CHAPTER VII

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SI

nti
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1°
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i

<

a "a

o.S
£8

c'=l- 1 SIS -IS -12

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^-1

Emaciated
but com-
fortable.

Dead.

Good.

Emaciated.
Able to
perform
only a
little
work.

Fairly com-
fortable,
but with
glyco-
suria.

fl

Symptoms con-
trolled by strin-
gent undemu-
■ trition.

Fatal acidosis pro-
duced by fast-
ing.

Improvement on
reduction of
obesity.

Condition imper-
fectly controlled
by diets too
close to verge
of tolerance.

Condition imper-
fectly controlled
by diets too
close to verge of
tolerance; no
apparent benefit
from treatment
of syphilis.

•tl
II

Severe.

Probably
moder-
ate.

Mild.
Severe.

Moderate.

n

1

i

1

Dangerous
weakness and
emaciation.

Loss of weight;
mo d era te
acidosis.

Loss of weight.

Gradual loss of
weight and
strength.

Gradual loss of
weight and
strength.

i

Careful dietary re-
striction, espe-
cially for last 6
yrs.

None for 4 mos.;
carbohydrate re-
striction for 3
mos.

None.

Spasmodic for 3
yrs.; undernu-
trition method
part of time for
2 yrs.

Various diets from
outset.

Buration of

diabetes

before

admission.

7 yrs.
7 mos.

6 "

Certainly
5, pos-
sibly 25
yrs.

<

§

<

yrs.
37

45

46

Between
31 and
41.

43

•nois
-snapc JV

C 5 !* ^ § §

•OJU 9B80

•^ O »-H 0\ t^
CS f*3 CSI lO VO

RESULTS — ^PROGNOSIS

549

a

O 4J

O

I"

Slag
a 2 S a £

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B

C3 ^^

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550

CHAPTER VII

1

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i55

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i^l^illl II l§lii

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Duration

of
diabetes
before
admis-
sion.

Si.

<

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e^ ^ 5 o

•uois
-simp^'nv

■ON 9S«0

EESXTLTS — ^PROGNOSIS

551

f

I

-a

o

o

O

on
utri-
tible
reat-
yph-

0

g ga°3

mprovem
slight
tion; no
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li

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o

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552

CHAPTER Vn

"§

a

i~i

>

':S

"^

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n

lO

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^

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g

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13 n T3 IT « t3

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g

a

s

o

1

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It III

O « o o

Duration
of diabetes

before
admission.

<

'lasuo :jy

i^

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£S s

•ON ssreo

m 11

EESULTS — ^PROGNOSIS

553

1

^

&4

lis

R I

?, ■^

Condi-
tion
Oct.,
1917.

^

'r'^

(^

. 1
II

1

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d en '.^ fl
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5S

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■ON ssoo

00

"O 1

554

CHAPTER Vn

TABLE IX.
Mortality,

Total
number

of
patients.

Dead.

Living.

Decade of
life.

No.

Per cent.

Average duration.

No.

Per
cent.

Average duration.

Under
treat-
ment.

From first
symp-
toms.

Under
treat-
ment.

From first
symptoms.

1
2
3
4
5
6
7
8

8
14
14
16
13

8'

2

1

5
9
9
5
3
2

62.5
64.3
64.3
31.2
23.0
25.0

mas.
8

16.5
13*

lot

2
3

vtos.
22

30.9
35*
24t
9
63

3
5
5
11
10
6
2
1

37.5

35.7

35.7

69

77

75

100

100

mos.

11

31.2

33t

28§

31

27

27

20

mos.
16
41.2
39t
81§
8611
63 f
142
Above 74.

Total or aver-
age

76

33

43.4

10.2

30.8

43

56.6

27.3

67.8

* Case No. 48 estimated.

f Cases Nos. 29 and 40 omitted.

I Case No. 38 omitted.
§ Case No. 7 omitted.

II Case No. 6 omitted.

\ Case No. 65 estimated.

At the same time, no hesitation is felt in discussing the results
from the therapeutic standpoint, even on the basis of the 43 per
cent mortality of the table.

First, if any defense of the principle of treatment is called for, it
sufi&ces to mention that the harmful effect of an increase of fat and
total calories has been proved upon a fair number of the cases and is
capable of proof in all the rest. None of these patients could be
treated successfully by former methods, and if 56 per cent have been
kept alive for the period in question, the figure represents ahnost
clear gain. Many of them would not even drag along for months if
overfed, but would die very quickly, as indicated by some obser-
vations in the preceding chapter.

Second, a critic may claim that this record at any rate justifies the
traditional pessimistic attitude toward diabetes, irrespective of tem-

RESULTS — PROGNOSIS 555

porary benefit by improvement in dietetic treatment. It may be
recalled that in the above tables, some cases formerly considered to
represent the extreme limit of severity have been ranked as mild or
moderate, and those classed as severe not only possess an actually
low assimilative power, but have also reached the stage of hopeless
inability to recover the lost power. A few milder, senile, obese, or
other cases had to be included as examples of their type. Otherwise,
broadly speaking (apart from rare cases with extraordinary sugar and
nitrogen excretion and acidosis, not always proving excessively severe
in the long run) the present series of cases is believed to be represen-
tative of the most severe diabetes that exists. The proportion of
examples of acutely threatening acidosis or complications, as tabu-
lated below, should also be borne in mind. The critic of the mor-
tality is invited to make comparison with the results in similarly
selected cases of any acute or chronic disease with any therapeutic
method whatsoever. It may be contended that in these other dis-
eases the patient who does not die is cured. But if sufficiently bad
cases be chosen for comparison, there are paralyses and other troubles
after diphtheria; there are recrudescences of syphilis, especially if the
choice includes a proper proportion of syphihtics too ignorant or too
careless to pursue treatment faithfully; and the worst cases of hyper-
and hypothyroidism are by no means all cured. The general medical
attitude toward these other diseases is not pessimistic, and a pessi-
mistic position toward diabetes cannot be founded upon the results
in the most severe cases.

Third, a glance at the mortahty table shows that the majprity
of the patients below 30 years die and the majority of those above 30
live. It may therefore be claimed that these figures at least confirm
' the inevitably bad prognosis of the severe form of diabetes in young
persons. The question to what extent there is such an inherently
hopeless severity in youthful diabetes, and to what extent merely a
greater sensitiveness to injurious influences, is discussed later in
this chapter.

In Table X, "under treatment" includes patients in the hospital
or following diet faithftilly at home; "without treatment" designates
those who have broken diet and died without returning to the hos-
pital. All the deaths can be classified under coma, compUcations, and
inanition.

556 CHAPTER vn

Under inanition are placed patient No. 1, who abandoned treatment
at home and gradually wasted away on a carbohydrate-rich diet which
apparently prevented coma; No. 4, a boy who was unduly undernour-
ished by mistake arising from his stealing food; No. 13, a child who
gradually progressed downward under inadequate treatment; No. 45,
a child received with incipient coma and extreme weakness and im-
possible to save on the latter account; and No. 54, a woman showing
continuous downward progress not checked by prolonged undernu-
trition. This last case was atjrpical, as was also case No. 8, in
which the necessity of gradual starvation was due to tuberculosis.
Under the usual conditions of treatment, even in the severest cases,
a necessary choice between death from diabetes and death from
starvation has not yet been encountered in this series, though it
may later have to be faced in a patient such as No. 73 and prob-
ably ultimately in some others.

Among the deaths from complications, those of patients Nos. 11
and 25 were clearly independent of the diabetes. The infectious
complications are discussed in connection with Table XII below.

The patients of this series are mostly such as typically die in coma.
With the single exception of patient No. 1, who starved to death on
starches and candy, every patient who broke diet died in coma, some
very qmckly. Where question marks are placed after the num-
bers in the table, the positive diagnosis was not obtained, but the cir-
cumstances made coma reasonably certain. No patient has gone
into coma while under the dietetic treatment. Since the principle of
treatment is to keep acidosis entirely absent, this statement means
only that the application has been feasible and successful. The only
exceptions to the general statement are patient No. 42, whose diet
was relaxed because of tuberculosis, and five others (Table X, first
column) whose treatment was incomplete, either because of initial
acidosis uncontrollable by fasting, or subsequent departures from diet.
These results indicate a genuine advance in the control or preven-
tion of acidosis; and that this is not confined to the present series
of patients but has become fairly general, at least in hospitals, is
indicated by the fact that a supply of levorotatory /3-oxybutyric acid
for experimental purposes is now decidedly more difl&cult to obtain
than formerly. Better success in the treatment of actual or threat-
ened coma is also indicated by Table XI.

TABLE X.
Causes of Death.

Case Nos. of patients dying of.

Coma.

Complication.

Inanition.

Under
treatment.

Without
treatment.

Cliaracter of complication.

Under
treatment.

Without
treatment.

1

2

4

8

. Tuberculosis.

9

10

11

Cardiac failure; perhaps em-
bolism.

13

15

18

25 .

Nephritis. Apoplexy (?).

30

34

Appendicitis.

36

37

38

Pregnancy. Pneumonia.

39

42

Tuberculosis probable.

45

46

Pulmonary gangrene.

48(?)

49

51(?)

52(?)

53

Some complication possible.

54

5S(?)

63(?)

69(?)

70

Influenza.

71

72

74

Tuberculosis.

Total

20

8

5

557

558

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560 CHAPTER VII

The majority of all the patients had marked acidosis when re-
ceived. There is no fixed boundary for the beginning of coma, or
between threatened or incipient and complete coma. Patients ex-
hibiting merely slight hyperpnea, malaise, drowsiness, or other pro-
dromes have been excluded from the above list. Only those have
been included who presented these sjonptoms in a degree sufficient
to make it evident to any observer that coma was actually beginning.
The standard of complete coma was not deep unconsciousness with
absent reflexes, since in some patients dying of acidosis such a stage
is absent or very brief; but when the patient was unable to compre-
hend where he was or answer questions intelligently, the condition
was classed as full coma.

The total number of such cases treated was 21, the deaths 7, or
33| per cent, the recoveries 14, or 66| per cent. It would be possible
to improve these figures by considering the fact that patient No. 38
came out of deep coma and died of complicating infections which
would have sufficed to cause death in a non-diabetic. There were two
deaths due to weakness; i.e., patient No. 45 recovered from incipient
coma on fasting, went intofuU coma when fed on account of weakness,
then came out of coma on fasting and died free from acidosis; patient
No. 71 entered in incipient coma, went on into deep coma before
fasting could take effect, partially woke up on continued fasting,
lived 9 days without fully regaining consciousness, and died in coma
when feeding was compelled by failure of strength. A number of
patients have entered with extreme weakness and emaciation, and
these features have not prevented treatment of the acidosis in any
adults of this series, for strength has usually been gained rather than
lost by such patients on fasting. Patients Nos. 45 and 71 above men-
tioned were small children, and the excessive weakness was the more
dangerous on this account. Fasting was risked because it offered a
chance, whereas without it death from acidosis seemed inevitable.

Complete Coma. — The chances must be considered to be strongly
against a patient in full coma under any treatment, and the results
in this series were more favorable than can be claimed as a rule.
Mention was just made of the two children (Nos. 45 and 71) who
came out of complete coma temporarily, also of patient No. 38, who
revived temporarily even in the presence of severe infection. Of the

RESULTS — PROGNOSIS 561

five examples of full coma at the time of admission, No. 25 was atypi-
cal and probably less grave in character. Patients Nos. 15 and 72
died after respectively 2^ and 7 J hours in the hospital. Patient No. 63
showed the lowest plasma bicarbonate and the most extreme collapse
of the series, and lived. It is possible that children go into and come
out from coma more readily than adults. In cases Nos. 38 and 71
with temporary recovery, and in case No. 63, the coma was complete
in the sense of absolute unconsciousness and loss of corneal reflex.
In the fatal case No. 15 there was no such stage. Patient No. 30 was
clearly conscious almost to the end, as frequently happens in fasting
acidosis.

Incipient Coma. — Excluding the two cases (Nos. 45 and 71) with
excessive weakness and the one (No. 38) with fatal infection, there
were twelve instances of patients received with incipient coma, with
one death. The recoveries include case No. 40, with coma im-
pending in the presence of lobar pneumonia. The fatahty was pa-
tient No. 39, who violated diet and was readmitted with extreme
dyspnea but perfectly clear intelhgence. There was abundant time
for treatment, but the methods were vacillating and uncertain, and
the patient went on into deep coma and died. This single death
was of a sort which will probably be avoidable when the treatment
under these circumstances is worked out better in certain details.

Alternate Feeding and Fasting. — -The last mentioned case was one
which apparently did not respond well to fasting. An example of
relief of fasting acidosis by protein diet was afforded by patient No.
37 at his third admission. The result of failing to recognize the con-
dition in time was shown by the death of patient No. 30. Protein-
carbohydrate diet is used for this puropse under the well known plan
of Joslin. Even protein-fat diet may sometimes serve, as illustrated
by case No. 35 (not in Table XI).

Alkali. — Patient No. 10 received 10 gm. sodium bicarbonate on
one day. Patient No. 64 received 25 gm. on one day only. Patient
No. 72 (first admission) was an example of treatment of threatening
acidosis without alkali. The high dosage of alkali given to patient
No. 1 was unnecessary in her case and in most cases. In certain in-
stances (Nos. 38, 40, 63) high bicarbonate dosage by mouth (40 to
125 gm. daily) has seemed both necessary and life-saving. In the
majority of the cases it appeared that fasting was the essential treat-

562 CHAPTER vn

ment and would have sufficed by itself, but that sodium bicarbonate
in moderate dosage (IS to 30 gm. daily, in doses of 5 gm. each) has-
tened the restoration of blood alkaUnity and the clearing of cHnical
symptoms. Joslin has rendered service in emphasizing the harm and
possible danger in the prevalent abuse of soda, and has demonstrated
the successful routine treatment of acidosis cases without alkali.
Patient No. 45 illustrated such injury from bicarbonate by mouth;
even with all the other factors against him, he might possibly have
recovered if he had not been thus dosed with alkali. Sodium bicar-
■ bonate intravenously failed to save any patients in this series (e.g.
No. 30). There was suspicion that a Uter of 4 per cent solution in-
travenously was responsible for the death of patient No. 1^, who
otherwise might have had a chance for recovery. It also seemed
likely that a somewhat smaller injection hastened death in patient
No. 39, who would have died anyway, and in whom the infusion was
tried only as a last resort. It is plain from the literature that some
patients have survived such measures in the past, but the danger of
large intravenous doses of alkaU should be more generally recog-
nized. There is also some evidence in recent literature that when
not enough alkali can be absorbed from the intestine because of
nausea, diarrhea, or other difficulty, smaller doses, perhaps 200 cc.
4 per cent sodium bicarbonate, may be given intravenously with
benefit and repeated at intervals of several hours. Most of the
truth about the real effect of alkali in treatment is yet to be learned.
It is certain that its wholesale use is pernicious. Also, it is probably
bad policy to try to force a low blood alkaUnity suddenly up to or
above normal by large alkali dosage, especially intravenously. Prog-
ress is favorable if the level of the plasma bicarbonate tends distinctly
even though gradually upward. A basic element of success in the
newer treatment of acidosis consists in allowing the organism time
and opportunity to adjust its disordered relations under the meta-
boUc reUef afforded by abstinence from food.

Infections.

One of the fears expressed concerning the undernutrition treat-
ment has been that the traditionally low resistance of these patients
would be reduced still lower, and that the favorable initial results

RESULTS — ^PROGNOSIS 563

respecting diabetes would in prolonged experience give way to a high
mortality from infections. The reverse has proved true. Table XII
includes all the important infectious complications encountered in the
entire series of 100 patients, except the 3 cases (Nos. 16, 41, 67) of
latent syphilis. The Ust includes 27 infections with 7 deaths and 20
recoveries. Noteworthy among the recoveries are 4 cases (Nos. 6,
40, 44, 62) of typical lobar pneimionia. Among the deaths, it may
be noted that normal persons sometimes develop conditions like those
in Nos. 34 and 38, and die from them, so that these results are not
necessarily attributable to diabetes. Patient No. 46 seemed to be an
individual of naturally low resistance, who might have succumbed to
pulmonary gangrene independently of diabetes. Also tuberculosis is a
leading cause of death among the general population, and it must not
be expected that diabetics shall be immune. Patients Nos. 9 and 12
were taken because of the suspicion of incipient tuberculosis, which
could not be definitely confirmed. It was possible by undernutrition
treatment of their diabetes, together with fresh air and light exercise,
to bring them into good physical condition, and pulmonary signs and
symptoms cleared up completely. The weak and emaciated condition
may be held chiefly responsible for 4 deaths, those of patients
Nos. 8, 42, and 74 from tuberculosis, and of No. 70 from influenza,
but this condition had resulted from the severity of the diabetes and
was not attributable to the therapeutic undernutrition.
The general experience may be summarized as follows:
First, efficient treatment of the diabetes, even though this involved
the most radical undernutrition, has seemed in every instance the
best treatment for the infectious complications. The results of abso-
lute fasting with carbuncle in case No. 27, with incipient gangrene in
case No. 17, with influenza in case No. 41, and with some of. the
pneumonia cases, are examples in point.^

Second, the susceptibility to either major or minor infections has in
no way run parallel to the degree of therapeutic undernutrition. The
great majority of the complications included in Table XII have been
present at admission or have developed on rather liberal diets. The
most radically undernourished patients of the series are not repre-
sented in this table. Also it might be shown by similar analysis of the

^ Benefit in cutaneous lesions has been reported by Grau, R., Cronica Medico-
Quirurgica de la Hahana, January, 1918.

564

CHAPTER VII

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RESULTS — PROGNOSIS

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566 CHAPTER VII

cases that common colds and other minor troubles have been most
numerous in the overfed patients. Presumably resistance is best in
the mildest diabetes permitting assimilation of a fairly liberal diet.
The patients who are worst off in susceptibility to and injury from in-
fections are those with severe diabetes on low diets which neverthe-
less slightly overtax their assimilative power. The experience indi-
cates that the resistance of these patients is increased by reducing
their nutrition within the limits of their assimilation. Also both
glycosuria and acidosis, which are the common accompaniments of
infection in inadequately treated cases, are frequently avoided when
the dietetic management has been thorough, as exempHfied by various
cases in this series. The vicious circle of aggravation of infection by
diabetes and of diabetes by infection is important to avoid. Patient
No. 42. might never have acquired tuberculosis had not tolerance and
resistance been broken down by unduly high diets, and the infection
in turn made the diabetes hopeless. Similar illustrations might be
pointed out in regard to less serious infections. The benefit of thor-
ough dietetic treatment consists not only in raising the existing toler-
ance and resistance, but in preventing them from falling lower.

Third, apart from the one case of pulmonary gangrene and three
cases of tuberculosis, none of the traditional complications of diabetes
has occurred in any of the 100 cases under treatment. The freedom
from pruritus may be mentioned as affording prophylaxis against in-
fection from scratching. Wounds have healed normally, and slight
accidents have never had serious consequences. It will probably
be conceded that under inadequate treatment the numerous troubles
hsted in older text-books are constantly overhanging every patient.
The relief from them is one of the greatest advantages of the present
treatment for both comfort and safety.

In conclusion it may be said that patients undernourished so as
thoroughly to control diabetic symptoms may be expected to display
a lowering of resistance corresponding to that of equally undernour-
ished normal persons. The large proportion of extremely under-
nourished patients enjoying complete freedom from infection, or re-
covering from occasional colds and other accidents like normal per-
sons, proves the safety and benefit of the undernutrition treatment
from this standpoint. Food in excess of the assimilation apparently
lowers resistance by poisoning the organism. Resistance is raised by

RESULTS — ^PROGNOSIS 567

increasing the assimilative power rather than the food supply. The
widespread contrary practice based on preconceived ideas is erroneous.

Reasons for Failure in Treatment.

At the outset of the present work, it was proposed' to take patients
solely on the basis of their diabetes, without regard to intelligence,
social position, or reliability of character. It was understood that the
statistics would suffer thereby, but it was deemed of interest to learn
what might be accompKshed with the average run of severely diabetic
patients. This policy has not been followed throughout, for especially
in view of the large number of applicants, there was an inevitable drift
toward choosing those who were most dependable and deserving.
The character qualification has been given a high place during the
last year or more. On the whole, however, the group has been fairly
representative; the patients have ranged from the ignorant shiftless
poor to the pampered willful rich; and some judgment is afforded
concerning the two influences discussed in the preliminary com-
munication mentioned; viz., the "human factor," representing all the
weaknesses of human nature, and the "scientific factor," representing
all the faults of treatment.

Table XIII classifies the failures of the present series, to the num-
ber of 52. On this basis, only 24 of the 76 cases rank as successes.
The failures may be divided into total and partial. The former are
reckoned at 40, viz. the 2>S deaths, and cases Nos. 6, 7, 14, 17, 22, 47,
and 56, in which abandonment of treatment makes a bad prognosis.
Partial failure is understood as downward progress or failure to
maintain the initial improvement. There are twelve examples. The
classification under fault of treatment does not always mean that the
treatment was mistaken. For example, a number of patients died of
coma or comphcations when no known methods could have saved
them, and in some instances diabetic treatment was not blame-
worthy because death was not caused by diabetes. But it is not
possible to distinguish sharply between deaths due to diabetes and
deaths independent of diabetes; also, when there is failure with no
fault on the part of the patient, it can only be said that the treatment

' Allen, F. M., Boston Med. and Surg. J., 1915, clxxii, 241-247.

568

CHAPTER Vn

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Death.

Downward progress.

Death.

Downward progress.

Relapse; bad prognosis.
Dismissed; bad prognosis.

Death.
It

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prognosis.
Death.

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diets; lack of blood analyses.
Unduly high diets.

Inadequate watching.

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Lack of self control; Christian

Science.
Poverty.
Too lax dietary regulations;

lack of blood analyses in

early period.
Neurotic character.
Too lax dietary regulations;

lack of blood analyses in

early period.
Ignorance.
Un trustworthiness; perhaps

drug habit.
Tuberculosis.

Deficient will and judgment.
Ignorance.
Cardiac disease.
Unduly high diets; inadequate

control of hyperglycemia.
Unreliable character.

Failure to relieve coma; un-
wise use of bicarbonate.

a

RESULTS — PROGNOSIS 569

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572 CHAPTER vn

was ineffectual to save him. The classification also does not mean
that treatment was perfect in the cases ranked as successful, or in
those where the patient is held solely responsible for failure. Also on
the patients' side it does not signify that those held guiltless never
took a piece of forbidden food, though some in the series can truth-
fully boast such a record. The serial numbers of the patients are set
down in columns according to the sole or primary fault on theix part
or on the part of the treatment. When contributing factors are
present they are set down similarly. The reason for the difficulty is
also epitomized as accurately as possible in the parallel columns.

Diabetes has been and is now probably the worst treated of all dis-
eases. The statement does not express so much the genuine difficulty
and mystery which have overhung the subject, as the failure to ac-
quire and apply existing and readily available knowledge. Space
does not permit enumerating all the faults on the part of the profession
at large. Mainly they are gross errors and carelessness in the kind
and quantity of diets prescribed, due largely to ignorance of the
underlying principles of metabolism and nutrition, and ignorance and
neglect of laboratory methods for early diagnosis and for control of
treatment. This history of the urine tests will doubtless be more or
less repeated with the newer blood analyses. Specialists cannot be
criticized for high caloric diets when these were considered proper.
But there is experimental proof that dogs cannot live on the ex-
tremely low protein, high fat diets such as specialists have considered
ideal in severe cases; yet they blamed patients for breaking these
diets. Also, how many specialists of the highest standing have sub-
jected patients to an intolerable regime in hospital and been thankful
to dismiss them as soon as glycosuria was absent or minimal, knowing
perfectly the immediate relapse that must follow, yet recording these
cases as "improved" and shifting responsibility for the subsequent
fate always upon the patient under one of two headings, either trans-
gression of the (impossible) diet, or "spontaneous downward prog-
ress"? The patient cannot begin to be blamed until he has been
made thoroughly symptom-free, on a diet which maintains him in
equilibrium in this condition and is otherwise feasible to follow, and
has been instructed adequately in the management of this diet and
in the routine urine tests. Such a program involves hardships in

RESULTS — PROGNOSIS 573

proportion to the severity of the diabetes, and a patient must have
the courage and will power to endure these hardships if he is to live.
He can be blamed if he breaks a diet which a fair proportion of other
patients have proved able and willing to follow.

Table XIII assigns the responsibility for accessory causes of failure
to patients and to the treatment in 9 cases each. The direct or
exclusive source of trouble is blamed upon the patients in 23 cases,
while in 29 cases the treatment was unable to avert disaster or there
were faults in its application. The commonest blunder was feeding
beyond the true tolerance and lack of thoroughness in controlling
h)^erglycemia and other symptoms. In less carefully treated cases,
it must hold in still greater degree that diabetics are more sinned
against than sinning.

One of the possible fears regarding an undernutrition treatment is
that patients wiU not consent to follow it. The actual experience
here and elsewhere has been that they adhere to these diets more
faithfuUy than to the former high caloric diets. Some temporary or
long continued (e.g. No. 57) successes have been achieved with indi-
viduals who had persistently broken orthodox diets. No patient
has been forced by hunger to transgress. The great majority of those
listed in the above table as disobedient have been on fairly liberal or
often high and varied diets, and were the sort of persons who would
not abide by any restrictions no matter how slight. On the other
hand, the most rigorously undernourished patients, like the majority
of the others in the whole series, have for the most part been faithful
and trustworthy; so that for every one who has transgressed it is pos-
sible to mention one or more who have cheerfully followed equal or
lower diets. Doubtless only a minority will bear permanently the
extreme restrictions requisite in the cases of maximal severity.

There is greater difficulty with half treated than with thoroughly
treated patients. The reasons are physical and psychical. The first
consists in the avoidance of true diabetic polyphagia, and of the in-
ordinate carbohydrate craving which comes from an overbalance of
fat in the ration. Simple hunger is much more easily and rationally
endured than either of these. Psychically there is the encouragement
and confi:dence of continuous sugar-freedom, along with absence or
diminution of the neurotic irresponsibihty which belongs more often

574 CHAPTER vn

to the active symptoms of diabetes than to the constitution of the
patient. One weak point of the dietetic treatment necessarily is its
dependence upon human nature. In general, diabetic patients have
proved agreeable and satisfactory to deal with. They have their
state of health in their own hands to a greater degree than any others.
Since diabetes affects the higher more than the lower grades of hu-
manity, wholesale charges against diabetics are the more improbable.
Many of them apply to their treatment the intelligence and resolution
that have brought them success in important fields of work. An unex-
pectedly high proportion of poor and uneducated patients have
shown the ability and willingness to carry out their diet efl&ciently.
The fidelity and cooperation on the part of a majority of children
with diabetes is remarkable. On the physician's side, success lies in
relieving patients of abnormal cravings and nervous states as far as
may be done by rational diet, and in estabhshing the necessary rela-
tions of personal confidence.

No hesitation is felt in acknowledging mistakes of treatment as the
cause of failure in a high proportion of cases. If anyone treating
such a condition as diabetes is not able in looking back over several
years' experience to see mistakes in his methods, it is a sign of lack of
progress. The errors in this series of cases have been chiefly of three
sorts. First, in the early cases, there were some mistakes carried
over from the older methods of treatment, and the uncertainty in-
evitable in beginning a new method. In particular, it was hoped
that the tolerance would rise if freedom from glycosuria and acidosis
were maintained for a prolonged period, and experience was required
to prove that in the genuinely severest cases such a rise is negHgible.
At this time, when both the clinical and animal investigations, and
especially the whole of the laboratory work, were carried by one per-
son without assistance, the necessary completeness of study was im-
possible. Second, there was some hope that exercise might permit
a higher level of diet and strength, especially if the blood sugar were
kept normal; and some injury was done before it was learned that
burning up calories by exercise is not fully equivalent to subtracting
them from the diet. Third, the independent basis of association of
the collaborators has given free scope to divergence of opinions and
methods. It has thus happened that the practice of feeding to the

RESULTS — ^PROGNOSIS 575

verge of tolerance, and the familiar attempt to "build up" patients,
especially children, have received a full and fair trial in a high propor-
tion of the cases, with consequences not profitable unless for their
instructiveness as experimental controls of the primary principle of
treatment. Readers looking for model histories will therefore find
few if any, but may profit Hke the authors from the record of blunders
and mismanagement, especially as most persoiis who have tried to
carry out the treatment have doubtless committed the same sort of
mistakes. Acknowledgment is always to be made of the shortcomings
of the treatment itself, inherent in its negative nature as a mere rest
for a weak function, without any positive element of cure. The feel-
ing is that the method has accomplished more benefit than could be
achieved by any former plan of treating diabetes, but that much
better results than those obtained in this series of cases are possible
in the future.

Severity of the Treatment.

The prompt effectiveness of fasting and undernutrition in controlling
diabetic symptoms has recommended the treatment in most quarters,
but has excited some misgivings in others. A requirement not always
fulfilled is that a critic should be able to furnish evidence that he has
carried out the treatment correctly in at least a few cases. Two fears
may be worth mentioning.

The first is the apprehension as to the suffering involved. This
may pertain to the initial fast or to the subsequent diet. The experi-
ence in this hospital has received abundant confirmation from
nimierous physicians and patients elsewhere, that the initial fast as a
rule is easily borne. In the severest cases the fast is an absolute
necessity, because less radical measures fail to control the symptoms.
In all other cases, dietary restrictions in proportion to the severity
are always necessary. Under former methods, weeks or even months
have been required to abolish symptoms in cases at all severe. Be-
sides the waste of time and money and the injury to the diabetic
condition by such prolongation of metabolic overstrain, there is
ample testimony that the long program is actually a greater tax on
the patient's endurance than is the brief fast. With regard to the
subsequent diet, it should be understood that the ideal is the best

576 CHAPTER VII

possible nutrition compatible with freedom from active S3miptoms.
Opponents must then support one of two theses : either that they can
bring about a higher assimilation without active symptoms by some
other method than by this method; or that patients wiU live either
longer or more comfortably when allowed to suffer the usual symptoms
of glycosuria, acidosis, and complications either in full force or in some
mitigated degree. It is believed that facts contradict both these
propositions. The latter is the one more likely to be defended by
those who seek to justify lax or careless methods; but it may be
pointed out that in this case they stand opposed to the best authori-
ties on diabetes from Naunyn to the present, who have held that
glycosuria and acidosis should be kept absent if possible.

A second question pertains to the possible danger or harm of re-
ducing the weight and nutrition of diabetic patients. The observed
facts have already been stated concerning subjective health and com-
fort, longevity, and the chance of infection when the patient is faithful
to diet. With regard to breaking diet, the conclusion was drawn
that this is less rather than more frequent under the new treatment.
The remaining question then is what is the effect of the treatment
when it is begun and later not followed out properly. A physician
clearly should not impose fasting if he is not competent to maintain
the benefit subsequently. When glycosuria is aboHshed by fasting,
then brought back by improper diet, then stopped by fasting again,
and so forth, the nutrition is lowered with no corresponding gain in
assimilation, and this harmful process may be continued even to
death from starvation. This is wrong management. When a pa-
tient abandons trealtment, there is a risk of arbitrary judgment
without tangible support. If he dies quickly, it may be claimed
either that the treatment injured him, or that it was the means of
prolonging life in a case demonstrated as severe by the outcome. If
he lives long, this result may be regarded as an after-benefit from
the treatment, or as proof that the stringent measures were unneces-
sary and that a longer and happier life was made possible by dis-
carding them. Confusion is largely obviated by considering facts as
follows. Nmnerous patients in the present series have been received
in critical condition, have been kept alive for long periods under
treatment, and have died in coma soon after breaking treatment, thus

EESTJLTS — ^PROGNOSIS 577

demonstrating the severity of the diabetes. When they have es-
caped early coma, they have lived surprisingly long for patients of
such a type; e.g., patients Nos. 1 and 60. As already mentioned, the
vast majority of deaths are due to acidosis and not to undernutri-
tion. To show an injury from the treatment, it would be necessary
to prove that patients are made more susceptible to coma by having
their acidosis completely cleared up. It is believed, therefore, that
careful treatment represents clear gain, even if it is later abandoned.

Prognosis.

The expression, by word or act, of opinion concerning the probable
course and termination in diabetes is more than prognosis ; it is a part
of the therapy. It is important that patients should be told the
actual truth, without favorable or unfavorable bias or concealment.
Great harm is frequently done by careless judgment of the earliest
and mildest cases and by an unwarrantably gloomy forecast in the
severe ones.

According to Naunyn,* "der Verlauf der Krankheit ist so verschie-
den wie denkbar." The statement is correct in the sense intended by
that author, signifying the wide extremes of mild and severe, acute
and chronic forms. It is not true in the sense of any bizarre hetero-
geneity of the disease, indicative of multiple organic origins or for-
bidding prognosis in individual cases. With allowance for the rare
exceptions encountered with every ailment, with consideration of the
principal factors of severity previously mentioned, and with cogni-
zance of the influence of aU three classes of foods, it is possible to out-
line fairly definitely the prospects in the great majority of diabetic
cases. Predictions can be hazarded to some extent at the outset,
but are more certain after a period of observation under treatment.
The prognosis of possible accomplishment under the present method
pertains to comfort and longevity.

If a patient can be kept alive, it is generally desired to know at
what level of comfort, strength, and efl&ciency this is possible. As no
cure exists, it should be stated plainly that this level is lowered in
proportion to the severity of the case. Tables I to VIII show the

^Naunyn, B., Der Diabetes melitus, Vienna, 2nd edition, 1906.

578 CHAPTER vn

existing condition of the patients of this series, which in the ma-
jority of those living is decidedly, and in many of them extremely
below normal. A point not to be overlooked is that, except for some
bad results due to transgressions by the patients or mistakes in treat-
ment, this state of invalidism had been present before and was bene-
fited by treatment, and the way to avoid such a state is to adopt
the most efl&cient treatment possible at the earliest possible stage. To
generalize the actual results, it may be said that the patients as a
whole have been relieved of the tormenting complications of dia-
betes. Therapeutic reduction of weight has ordinarily been attended
by increase, not by diminution of strength. ' The notions of " starved"
patients entertained by those having no experience with the method
are widely erroneous. Of 18 living patients above the age of
30 who have been faithful to diet, (excluding the cardiorenal case
No. 61), all but 2 are carrying on their regular duties more or less
satisfactorily, and 13 of these are almost or entirely free from
impairment of strength,, working power, appearance, or subjective
health referable to diabetes. The most extremely undernourished
man (No. 24) has carried on his business continuously. The most
radically undernourished woman (No. 60) has continued light house-
hold tasks and supervised the bringing up of her daughter. There is
frequently a tendency to progressive gain in health in this older
group. Of the 5 in the third decade counted as living, one was
an exceptional case resulting in apparent cure, one is emaciated by
reason of transgressions of diet, one looked and felt well at departure
to Finland, and two are leading their usual lives in such condition
that a stranger would notice nothing wrong, over 3 years from the
onset of their diabetes. The younger patients are discussed more in
detail below. The best accomplished in them has been to preserve
such strength and well-being as they possessed at the time of begin-
ning treatment.

A familiar defense of overfeeding is that the patient must die any-
way and should be kept as comfortable as possible in the meantime.
Very often this is a mere excuse for mismanagement, and it is not
justified by the present experience. No patient of this, series has
broken diet with impunity. The penalty of eating much or little in
excess of the tolerance has been corresponding reduction not only

RESULTS — ^PROGNOSIS 579

of length of life but also of strength and comfort. Cases mild enough
to drag along for months or years on improper diet are also mild
enough for a reasonably satisfactory diet and bodily condition under
proper treatment. The more severe cases face a correspondingly
worse dilemma. Moderate overeating does not satisfy; diabetic
polyphagia is harder to endure than simple hunger, and the malaise
of chronic acidosis and the troubles of various complications are super-
added. Excessive overeating of carbohydrate increases polyphagia
and emaciation; excessive overeating of fat brings quick coma. The
only argument against thorough treatment must therefore be that
it is cruel to prolong the state of impaired health. But euthanasia
is no more justified in diabetes than in numerous other conditions.
The strongest reason for the earliest and most efl&cient treatment
possible is not the relief of the immediately threatening or trouble-
some symptoms, but is rather the fact that such treatment acts to
preserve strength, comfort, and assimilative power, and either saves
from the condition of extreme privation altogether or holds it off
to the farthest possible time. Diabetics who overeat for the de-
liberate purpose of killing themselves are uncommon. In this re-
spect the experience shown in Table XIII probably holds for diabetics
in general. The patients who died from breaking diet were not
driven to desperation by hunger or suffering. They were generally
not the ones who had to endure the greatest privations. , They were
rather the ignorant, the careless, the weak-willed, the neuropathic,- and
others who would not have been faithful to any restrictions no
matter how mild. Under such circumstances it is the physician's
duty to strengthen, encourage, and aid. The condition of the living
patients of the present group, young and old, ranges from perfect
subjective health to very serious privation, according to the severity
of their diabetes. The lesson from the standpoint of comfort is
wholly in favor of efficient treatment at the earliest possible stage,
not in favor of bad treatment at any stage. The only apology for
reciting these obvious facts is the frequency with which the fallacy
in question is encountered.

As to the prognosis for preservation of life. Tables I to DC
show the high mortality of 43.4 per cent as what the physician
may expect if he limits his practice to cases like these. For dia-

580 CHAPTER VII

betic patients themselves, it is instructive to extend the inspection to
Table X. Two or three elderly patients have paid for breaking diet
only in loss of health and not by loss of hf e. Otherwise,- the record
stands that the patients who abandoned treatment died, all but
one of them in coma. This statement is unjust in a few instances
where patients only gave up because of discouragement after down-
ward progress; but it can still be answered that none of them had
been called upon to endure lower diets than others have successfully
endured. If the list be limited strictly to those who have faithfully
followed treatment throughout (and they are the majority) then only
fourteen deaths remain to be explained. Of these, three (Nos. IS,
30, 45) were acute deaths, due to coma immediately following admis-
sion to the hospital for commencing treatment. Nine were due to
complications (tuberculosis in Nos. 8, 52, 74; heart disease in No. 11;
nephritis in No. 25; appendicitis, pneumococcus infection, pulmo-
nary gangrene, and influenza in Nos. 34, 38, 46, and 70). No. 13 was
complicated with urinary calculi and the diabetic treatment also was
not thorough. No. 54 was an unusual case, with fatal course sus-
pected as due to some complication. If all these cases were set aside,
it would make an absolutely clean record without deaths in the en-
tire experience of 3| years. Of course it is not permissible to wipe
the slate clean in this manner. For example, the tuberculosis in case
No. 52 was clearly the result of bad progress of the diabetes under
wrong treatment; the influenza in case No. 70 was probably fatal
chiefly because the patient was weak from diabetes. On the other
hand, some deaths from complications were, as stated, apparently
independent of diabetes. The fact may further be noticed that
diabetic statistics are perhaps the only ones in which patients who
do not follow the treatment are included among the failures of the
treatment, even when, as with most of the disobedient ones here, the
fault was solely their own. This exception with respect to diabetes
is just, because one important test of the practical worth of a treat-
ment is its feasibility, not for some specially selected patients, but for
the general average of human nature. Nowhere more easily than in
diabetes is it possible to obtain that famihar form of therapeutic
data which in themselves are not false, but are so selected as to lead
to erroneous conclusions. It can be repeated that in the^choice of

RESULTS — PROGNOSIS 581

these cases, all pains were taken to invite the highest mortality pos-
sible. It is fair to claim that disobedience, coma, and complications
do represent special difficulties. From the medical standpoint all
the deaths and failures from all causes belong strictly in the series,
and they were given full weight in the foregoing account. From the
patient's standpoint, however, it is justifiable to point out that if he
is constantly faithful in treatment, if he has not died in coma at the
outset, and if he is not one of the small proportion (9 or 10 in 100
cases in this series) to succumb to complications, his chance of sur-
vival according to the above statistics to date would be close to 100
per cent. These figures apply to a group of cases of high average
severity, in which coma, complications, weakness, and other dangers
are most common; also it was noted that there was considerable in-
jury from mistakes in treatment. It is believed that the record
offers a hopeful outlook for the average diabetic patient under efficient
care. It wiU not be possible to keep patients with the severest dia-
betes alive indefinitely by this or any other dietetic treatment, but
the great prolongation of life in them shows how much may be
hoped when such treatment is applied in the earliest and mildest
stages, as it properly should be.

" Spontaneous Downward Progress."

The belief in an inherent progressive tendency in at least a large
proportion of diabetic cases is universal. The evidence in the litera-
ture is valueless. The belief rests largely upon the rapidly fatal
course of many severe, especially youthful, cases. Other instances
cited, as by Naunyn, are merely those in which glycosuria was sup-
pressed by carbohydrate restriction and returned on the usual high
caloric diet. This question of spontaneous downward progress may
rank as the most important one in the entire subject of diabetes,
from two viewpoints. The first is clinical. It is the question of the
possible prolongation of life; whether, with adequate regulation of all
classes of food and aboHtion of aU symptoms, the diabetic process is
brought to a standstill, or is merely slowed so that the fatal end comes
somewhat later but just as surely. The second pertains to the path-
ology and etiology of diabetes; whether the cause producing the
diabetes is a transitory or a continuous and progressive process.

582 CHAPTER vn

Knowledge on this point would decide the clinical prognosis. Con-
versely, observations of the progress of patients with relief from food
injury will throw much light on the nature of the diabetic process.

From one aspect, it might seem natural to anticipate that, since
diabetes is not actually caused by diet, the essential process should
not be halted by change of diet. This point could not be settled
except by an anatomic investigation, as described in the following
chapter. This pathologic study has shown that the downward prog-
ress due to food injury is an additional and separate process, inde-
pendent of the original cause of the diabetes. A standard object of
comparison is the partially depancreatized dog. Here a surgical
resection produces a definite degree of pancreatic deficiency, and the
absence of any inherent progressive tendency has been established by
prolonged experiments. More or less gain in assimilation maybe
observable, dependent in at least some cases on h)^ertrophy of the
pancreatic remnant. But when a fairly fixed limit of tolerance has
been determined for some time, this shows little further spontaneous
change in experiments extending over years. The behavior in this
respect is like that of many human diabetics. The most important
point is that in suitably prepared animals with rather severe dia-
betes, the. prevention of active symptoms and fatal result requires
restriction not only of carbohydrate and protein but also of total
calories and body weight. By addition of fat to a diet on which the
condition is demonstrably stationary, the "spontaneous downward
progress ' of clinical cases can be precisely imitated. Even with
milder diabetes, it is possible to prove the same relation between
weight and tolerance as exhibited by human patients There are
dogs now living whose tolerance can be varied at any time by manipu-
lating their body weight.

The pathologic evidence needs to be supplemented by clinical ob-
servation. It is obvious" from the former that pancreatitis is some-
times chronic and progressive; also, even an acute inflammation
starts up changes which continue to a variable time and degree.
Such a process is necessarily beyond the power of dietetic treatment.
Clinical experience must therefore decide what proportion of human
patients show indications of such an advancing lesion, or any other
progressive factor not present in dogs and independent of food injury.

RESULTS — PROGNOSIS 583

The present series of cases should have answered this question, and
the greatest disappointment of the clinical research has been the
inability to carry out the original plan to this end. The existing
observations are presented for the partial information which they
afford. As mentioned before, the aggravation resulting from infec-
tion was exhibited by patient No. 8 with tuberculosis, and by other
patients with various acute infections. Similarly, patient No. 54
was a typical example of downward progress according to the idea
which has been so prevalent. When freed from symptoms by radical
undernutrition, it was impossible for her to remain so on any living
diet; the sjonptoms kept recurring in spite of progressive reduction of
weight and metabolism ; there seemed to be nothing but a continuous
choice between inanition and coma, and the patient finally died
after a steadily losing fight of 9 months. This is the conception which
has existed in some quarters concerning the undernutrition treatment
of severe diabetes. It is possible that some progressive process was
at work in this case. It is certain that the other cases of the series
have not been of this sort. The experience with the others can
best be considered in the groups above the age of 30 and in the
decades below that.

In the patients above 30 years, it may not appear surprising that no
progressive downward tendency has as yet been observed. Yet the
older patients are the ones in whom the pathologic studies in the lit-
erature have shown chronic pancreatitis most frequently. If there
were a progressive decline clinically, it might be readily explained by
progress of the pancreatic lesion, and some cases must certainly
show such a decline ultimately. In view of the known pathologic
findings, the accepted favorable prognosis of diabetes in the elderly is
rather remarkable. Patient No. 24 is a man aged 44 years, with the
most severe diabetes of any man of this group, and with the typical
history of the disease beginning in mild form 7 years previously,
and gradually progressing to the extreme stage present on entering
this hospital. There was a history of indigestion, pale feces, and
jaundice in the year prior to the diagnosis of diabetes. The skin is
yellowish, there is a dyspeptic tendency, and especially fat easily
upsets the digestion. The prediction can be made that if autopsy is
obtained it will reveal chronic pancreatitis. The case has actually

584 CHAPTER vn

shown the stationary tolerance characteristic of severe diabetes, and
has done well under the circumstances during ahnost 3 years of ob-
servation. The woman No. 60 had the severest diabetes repre-
sented in this group. The type was more like that of younger per-
sons. Within less than a year after onset, the condition had attained
such severity that only the most radical undernutrition was able to
control it. Even though her hyperglycemia was not thoroughly
controlled, the downward progress was apparently halted, and there
was no perceptible further loss of tolerance during nearly 2 years of
observation. The improvement manifested by other patients when
their weight was reduced has persisted with continuous regulation of
diet and weight. Particularly important are the observations with
patients such as Nos. 23 and 41, showing how assimilation rises and
falls inversely with the weight, just as in dogs. Though such cases
belong among the milder ones of the series, it is plain that "spon-
taneous downward progress" can be produced in them at any time by
the familiar "building up" in diet and weight. With reUef from
such an overload, they have shown generally an upward tendency
as far as the period of observation extends.

In the third decade (cf . Table III) a number of cases are of service
only as examples of the rapid downward progress resulting from
dietary errors. The cases with compUcations are excluded; none
showed downward progress prior to the fatal infection. Patient No.
40 apparently illustrated complete recovery from acute diabetes ac-
companying pneumonia. Patient No. 29 was lost from observation.
No. 54 was the atypical case above mentioned. This leaves Nos. 1,
3, 32, and 52 as suitable for the present discussion. All showed more
or less downward progress. No. 3, for example, had been a very rap-
idly progressive case, with active glycosuria and acidosis under the
previous treatment and with the prognosis of only a few months of
life. A consistent reduction of diet and weight was maintained during
the 3| years since. With the mistakes in diet known to have oc-
curred in hotel life, causing slight glycosuria at times, it is not sur-
prising that some decline of tolerance has occurred in such a case;
but this has been slow in proportion as the dietetic errors have been
sKght. The other three patients illustrate the effects of continually
feeding to the verge of tolerance, keeping up continuous hyperglycemia

31ESULTS — ^PROGNOSIS 585

and occasional glycosuria. In dogs, one of two things occurs under
these circumstances. One possibility is that the pancreas remnant
increases in size or function and hyperglycemia diminishes and dis-
appears. This is the result which is noticed frequently in the more
elderly patients, and which originally was hoped for in others. The
other possible outcome in dogs is a gradual breakdown of function
under the overstrain when the pancreas is unable to rally in this
manner. This breakdown is much slower than on a higher diet,
but the susceptibility to this injury is in proportion to the real severity
of the diabetes. Accordingly the youngest patients are generally the
most susceptible. There is nothing perceptible in this group of cases
that cannot be exactly imitated in dogs.

In the second decade (Table II), case No. 4 illustrates the fact
that not all patients can be classified together in prognosis merely
because of youthful age. This diabetes began at 5 years; the diet
was the conventional sort on which children ordinarily die quickly,
and there were frequent transgressions; yet the boy lived to the age
of 12. There is natural interest as to what might have been the
result with this child if all active symptoms had been kept absent by
eflBcient dietary regulation from the outset. Several of the other cases
illustrate the rapid downward progress caused at this age by disregard
of diet. One of these. No. 10,^ showed "total" diabetes, as demon-
strated by the D : N ratio and the respiratory quotient at the time of
his admission. The gradual marked gain in food tolerance represents
upward not downward progress, in contrast to what quickly hap-
pened when he abandoned restraint. In the history of case No. 2
(Chapter III) it was pointed out how rapidly aggravation was pro-
duced by each departure from diet, whUe in the long intervening
periods in the hospital the absence of any perceptible downward
tendency was demonstrated, even though the treatment was far
from ideal. The patients of this group who were fairly faithful to
diet can be divided into those received in the final severe stage of
diabetes, and those received in an earlier, mUd or moderate stage.

The former group consists of cases Nos. 13, 26, 62, and 63. The
faults in their treatment are pointed out in the histories. In par-

^ Gerald S. in the paper of Allen and DuBois.

586 CHAPTER VII

ticular, hyperglycemia was kept up almost continuously by diets too
close to the verge of tolerance. The important feature is that they
had already reached the stage where improvement to the extent of
tolerating a high diet was not possible even temporarily. There-
fore, to avoid glycosuria and acidosis, all were limited to low diets..
Two are alive, and two have recently died, after periods of 8 months
to nearly 3 years under this treatment, and 20 months to 6 years of
total duration of diabetes. More or less rapid downward progress
was evident in all before beginning this treatment. It has since
been not perceptible in two, and has been slow in the other two, due
to obvious mistakes and accidents. The result is the more remark-
able because dogs with similarly severe diabetes would have been
dead long ago if treated in this fashion. An inherent downward
tendency is therefore not revealed.

The cases in the mild or moderate stage comprise Nos. 28, 37,
42, 64, and 66. Patient No. 28 improved decidedly during hospital
treatment with undernutrition which reduced her weight by 1 kilo-
gram. She was allowed high diets after discharge, and has grown and
developed normally and gained markedly in assimilative power.
Experience here and elsewhere has proved that the result of such
high rations in diabetic children is almost always disastrous; and it is
a fair inference that this case was somewhat unusual in t5^e, prob-
ably the result of an acute infection, and more or less comparable
with the adult case No. 40, where there was apparently complete re-
covery from diabetes accompanying pneumonia. The prognosis for
this child was almost certainly unfavorable if active symptoms had
been allowed to continue. With the aid of temporary undernutri-
tion the expected downward progress was changed into upward
progress, and the result is a thoroughly comfortable and normal
appearing child, whose improvement may perhaps continue further
to an unknown extent. On the other hand, trouble may yet result
from her heavy diet, occasional transgressions, and hyperglycemia;*
and there is further the question how much more rapid and com-
plete her recovery might have been to date if the diets had been
more prudent.

* As noted in the history, this patient on excessive diet has suffered relapse, as
feared.

RESULTS — PROGNOSIS 587

Of the four others, patient No. 64 was a boy of 11 years, with the
most acute form of juvenile diabetes, threatening coma within 3
weeks of the first observed symptoms. His history shows the rapid
improvement with undernutrition, the abiHty to tolerate 50 gm.
carbohydrate and 1750 calories at discharge proving that the actually
severe stage had not yet been reached. The tendency of the blood
sugar to fall to normal was reversed by the unwise increase in diet.
The initial improvement was therefore not maintained. In conse-
quence of a relapse, the diet was reduced to 1250 calories, still with 50
gm. carbohydrate. This ration might have been tolerated at first,
but is now too high, as shown, by the persistent h)rperglycemia, and
further relapse will occur unless the treatment is changed. Patient
No. 42 was a girl, also aged 11, and with diabetes of 3 weeks duration.
The glycosuria and acidosis were controlled by undernutrition as
usual, and the blood sugar also was brought to normal. She was 232
days in the hospital, and the great and genuine improvement during
this time was beyond question. She was then overnourished so that
the original weight was regained, and was allowed a diet of 1500 cal-
lories, averaging 48 calories per kilogram, at discharge. The warning
of the subsequent hj^erglycemia was not properly heeded, and the
inevitable relapse followed. The diet then had to be cut to 800 ca-
lories; i.e., as usual, both food and body weight were made lower than
would have been required for proper treatment at the outset. Even
so, the measures were not rigorous enough to control hyperglycemia,
and the characteristic downward progress continued, until terminal
tuberculosis closed the failure. The story of patient No. 37 is similar.
He also had diabetes of 3 weeks duration, which had already brought
him to the verge of coma. With him also the s}anptoms were abol-
ished by undernutrition and the blood sugar was reduced to normal.
The inherent power of recovery was so great that a tolerance for over
400 gm. carbohydrate was regained in hospital. Here also undernu-
trition was abandoned, an average ration of 43 calories per kilogram
was prescribed at discharge, and at his second admission he showed
a gain of 6.2 kilograms weight and a corresponding h)^erglycemia.
The diet was then somewhat reduced, but not enough to stop the
downward progress. The subsequent history and fatal termination
were the famihar results of a "building up" policy. The fact is

588 CHAPTER vn

noteworthy that these patients, taken in the relatively mild stage of
their diabetes, with demonstrated capacity for improvement in
assimilation, are dead, while patients of the fomjer group, taken in
the stage of severe diabetes after practically all power of regaining
tolerance had been lost, have survived after a corresponding interval
of time. The evident difference is that those with severe diabetes
were kept on low diets perforce, for fear of glycosuria and acidosis,
whereas in the milder cases the manifest tendency toward recovery
was abused by overloading with diets such as could only be justified
on the assumption that a short period of undernutrition had practi-
cally cured the diabetes. The difference is plainly not one of the in-
herent progressive nature of the cases; for some of those showing the
most alarming initial tendencies have displayed the most marked
power of recovery under treatment. The truth is that fuU recovery
is very rare, and the method of undernutrition, by which the initial
success is gained, must be followed in the later treatment in propor-
tion to the requirements of each case, if success is to be achieved.
Additional support is given to this principle by comparison of the
remaining case No. 66 with those just described. The parallelism
and contrast are particularly strong between this and No. 37, as de-
tailed in the previous chapter. Greater severity of the diabetes in
the girl No. 66 was seemingly indicated not only by the lower carbo-
hydrate and total food tolerance, but also by the practical absence
of the power of improvement. Precautions with respect to total diet
and body weight were observed with this patient. The boy No. 37
died at the end of 2 years of diabetes, while the girl No. 66 after 2
years suffered not the sHghtest diminution in health or tolerance.
Further evidence is afforded by the fact that unduly high diet or
body weight has in each instance given rise to hyperglycemia in the
girl, whereas by limiting these her blood sugar is kept normal. It is
evident that diets much lower than those imposed upon the boy
would in her case eyen more quickly produce the "spontaneous"
downward progress. It is certain that by the difference in treatment
in her case, the aggravation to which she is clearly susceptible has
either been prevented absolutely, or reduced to such a minimum
that it is not perceptible within 2 years.

RESULTS — ^PROGNOSIS 589

The cases in the first decade (Table I) in which treatment was fol-
lowed sufiiciently to permit judgment on this point, are also divisible
into those received in the severe and those received in the mild or
moderate stage. The only representative of the former is case No.
73. The history of this 3 year old girl is that 1 year before admission
she received treatment for her diabetes in its incipiency. She was
then allowed the high diet which she could apparently tolerate, and
within 10 months marked downward progress was manifest. Strin-
gent reduction of diet was necessary in the severe stage, and though
the treatment has been imperfect, no further downward progress
has been perceptible in the subsequent 10 months.

Patients Nos. 55 and 68 were babies aged respectively 26 and 23
months, with early but intense diabetes. The symptoms were con-
trolled as usual, and then undernutrition relaxed, the diets at dis-
missal averaging respectively 3.8 gm. protein and 48 calories, and 5
gm. protein and 68 calories per kilogram. In the light of experience,
nothing but downward progress could have been expected, since chil-
dren generally show no greater power of recovery than older pa-
tients. Both children finally died after the parents had given up the
diet from discouragement. It can only be claimed that by this in-
adequate treatment the downward progress was slowed. • Patient No.
76 is a boy aged 4 years, likewise with diabetes of about 3 weeks du-
ration. His diet has been such as to prevent him from gaining weight
unduly. He has been comfortable, active, and of healthy appear-
ance, his blood sugar has been kept normal, and he has certainly
not lost and apparently gained considerably in assimilative power
during 8 months. This case seems unquestionably to be of the type
which ordinarily progresses very rapidly to a fatal end, but there
has as yet been no perceptible sign of any "spontaneous" tendency,
unless it be upward.'

Accordingly in the first and second decades of life, when the prog-
nosis is supposed to be worst, there have been altogether 13 patients
in this series who have followed diet to a reasonable extent. The
deaths have been five in number, or 38.5 per cent. The hving ones
number eight, or 61.5 per cent. The average duration of the five
fatal cases under treatment (to October, 1917) was 20 months, the

'The favorable condition is still maintained (June, 1919).

590 CHAPTER VII

average duration from the first diabetic symptoms 25 months. The
average duration under treatment in the eight living patients has been
20 months, from the first known symptoms 69 months. Mention
was made of the part played by mistaken management in all the
fatal cases and some of the living ones. Nevertheless the figures are
better than any reported for cases of this type under any former
method of treatment, and contradict the time limits heretofore set
for juvenile diabetes. An outstanding feature is that even the
childish patients have displayed actually greater resistance to the
injury of overfeeding than dogs with correspondingly severe dia-
betes. It must therefore be concluded that as yet no spontaneously
progressive tendency has been demonstrable in any of these cases.

Such a conclusion, if confirmed in the future, will possess scientific
importance in relation to the etiology and pathology of diabetes. It
will not necessarily assure therapeutic success. Transgressions of
diet, infections, and the demands of growth are among the dif&culties
to be thought of, independent of any specific progressive process in
the pancreas or elsewhere. It can only be repeated (1) that chil-
dren as a rule make good patients; (2) that infections are most fre-
quent and work greatest havoc when the diet is wrong, and are fewest
and least harmful, often leaving no lasting injury to the diabetes,
when the dietetic management is right.

There is always the possibility that sufiiciently prolonged observa-
tion wiU yet reveal an inherent progressive tendency in some or most
cases of diabetes, especially in youth. It has also been freely con-
ceded from the first that no known dietetic treatment can enable
children with the severest diabetes to grow and develop normally.
It is a gratifying surprise that the weakened function can bear the .
strain of the high metabolism of childhood as well as it does. It is not
feasible to fix any theoretical standard as to what ration a diabetic
child must take. The safe level of diet and weight necessarily varies
with the severity in different cases. Maintenance at reduced weight
is possible on rations far below current text-book stipulations, be-
cause undernutrition acts powerfully to reduce metabolism even in
children. The rule followed at present is, after controlling glyco-
suria and acidosis by fasting, to work up to 1.5 to 2 gm. protein per
kilogram, enough carbohydrate if possible to keep acetone reactions

RESULTS — PROGNOSIS 591

negative in the urine, and finally such fat and total calories as can
be borne without either acidosis or hyperglycemia. Possibly the
metabolism may sometimes have to be brought as low as that of nor-
mal adults or lower. The observations do not yet permit generaliza-
tion as to what happens with the growth of such children, or whether
undernutrition is the sole retarding influence or whether a specific
diabetic defect plays a part. The unfavorable prognosis for develop-
ment in the extreme cases should not be too rashly extended to juvenile
diabetes in general. Apart from the very mild or transitory examples
occasionally described in the literature, it may be noted that out of
eight early but intense cases in this series (Nos. 55, 68, 76, 28, 37, 42,
64, and 66), three (Nos. 28, 66, and 76) are indistinguishable from the
normal in appearance, and the high capacity for improvement ex-
hibited at first by Nos. 37, 42, and 64 suggests the possibility of really
satisfactory results, had they been granted a fair chance in their later
treatment. Under any interpretation, these figures to date offer a
prospect of growth and development in a higher proportion of cases
of juvenile diabetes than admitted heretofore.

It will probably prove erroneous to group all cases of youthful dia-
betes together in a common prognosis. Rare cases as mentioned in
the literature are transitory in spite of unregulated diet. A few
others have recovered completely after prolonged conventional treat-
ment. It is reasonable to believe that still others will recover more
slowly and incompletely, and the ease and extent of such recovery
may be governed by the treatment. As suggested above, patient No.
28 might have died under former treatment, and the actual result
might have been better had the treatment been better. Others may
possess little or no power of improvement in assimilation, and growth
and development may have to suffer in proportion to the actual
deficiency of metabolic function, and downward progress may even
occur in spite of any dietetic treatment. The outstanding feature of
present observations in this connection is that this unfortunate con-
dition of minimal food tolerance and absent recuperative ability,
with the accompanying dark outlook for growth and development,
was practically always the consequence of improper feeding in the
earher stage. It ought to be self-evident that not food, but the
power of normally assimilating food, is the essential thing which

592 CHAPTER vn

diabetic children lack; and the best growth and development are ob-
tained by the method which best conserves and strengthens their
assimilative capacity. Success does not lie in trying to force them
with any kind or quantity of food in excess of the true tolerance.
Universal experience has proved that on such an overfeeding plan,
what develops is the diabetes and not the child. The same principle
applies to the nutrition of adult patients. It is the more important
since there is now evidence that excessive diet can produce actual
anatomic destruction of islands of Langerhans.

Whatever the truth may prove to be concerning spontaneous tend-
encies in diabetes as revealed by suflEiciently extensive study, it has
been urgently necessary that this question be raised and investigated.
"Spontaneous downward progress" has been the excuse for every kind
of mismanagement, blimder, and failure of diabetic treatment in the
past. The present work, though not competent to exclude such a
process, does prove decisively that it is generally no more than a
minor factor, even in cases of the worst type. The traditionally
rapid course of diabetes in infants and children indicates not an in-
evitably acute process in them, but rather a high degree of suscepti-
bility to breakdown of their islands and their assimilation by over-
strain. The danger is increased by their naturally high metaboUsm,
which would fatally injure the tolerance in any adult with severe
diabetes.

The most important therapeutic lesson is the need of limitation of
the total diet and metabolism with care proportioned to the potential
severity of the case. For this reason it is important that children and
all others subject to severe diabetes should come under the care of a
competent specialist at the earliest possible moment. Practitioners
at large may do well to limit themselves to the care of the milder dia-
betes of older persons, always with the understanding that this also
requires no small study and attention. For the young patients their
greatest service will consist in the earUest possible diagnosis, and, if a
speciaUst is not close at hand, the initial control of symptoms by
fasting and low diet. This stage is generally comparatively simple;
the real difficulty comes in planning a diet which shall be practicable
to support life while guarding as effectively as possible against down-
ward progress. A tremendous amount of damage is commonly done

RESULTS — PROGNOSIS 593

to these patients at the time when the therapeutic results are imag-
ined to be most brilliant. It is extremely important to realize that
such injury is absolutely irreparable according to present knowledge.
The high tolerance, the capacity for improvement, the chance for
growth and development, which may be present at the time of the
first diagnostic symptoms, have been lost when the young patient,
after a period of unskilled handling, is finally sent to the specialist
to save him from imminent death. Notwithstanding the suggested
limitation of the r61e of the family physician, it is evident that some
country doctors are treating diabetes better than some specialists.
There can be no possible restriction against anyone willing to equip
himself with the necessary technique and training. But the fact is
that the best diabetic treatment does require laboratory equipment
and the ability to use it, together with rather exceptional knowledge
of metabohsm and a fair experience with diabetes itself.

Three desirable aids to the success of practical dietetic treatment of
diabetes may be named in order of importance as follows: (1) Early
diagnosis and prompt use of the necessary measures on the part of
the general medical profession. (2) Competent specialists and con-
sultants, with properly equipped hospitals, clinics, and dispensaries,
for the treatment and instruction of both rich and poor patients.
The diabetic classes in coimection with clinics in some cities are an
important advance. (3) Institutions where diabetics may live or at
least board continuously when they' need and are willing to follow
careful diets but have not the facilities or means to obtain them. The
opportunity to support themselves by work within their abihty would
be a great assistance. Only a small proportion require as long hospital
treatment as the very severe cases of the present series, but neverthe-
less hospital care should be longer than is the general rule. The
process of discharging as soon as symptoms are relieved and read-
mitting for successive relapses is fatal. Improved treatment merely
prolongs the misery when continuous after-care is prevented by ig-
norance or poverty. Patients could sometimes support their fami-
lies if they could have the right work in the right environment, when
without it the outcome is disastrous for them and their families. The
need is real, but it is difficult to formulate concrete suggestions for
relief.

594 CHAPTER VII

General Summary.

The preceding chapters show that the acutely threatening sjonp-
toms of diabetes have been controlled by the present treatment in
a successfid and radical mannef which bears comparison with the
most powerful therapeutic measures for any acute or chronic disease;
but the diabetes is not cured, and downward progress occurs in prac-
tically aU potentially severe cases unless the same priuciple of limita-
tion of the total metabolism and body weight is adequately observed
at all times. Exercise and some approach to a normal existence
have been found possible and beneficial generally even in the severe
stage. The most potent cause of aggravation of the condition is
overfeeding; and since carbohydrate and protein have long been lim-
ited, by far the greatest harm in recent times has been due to the
customary excesses in fat and total calories. The unwise use of fat
can give rise to glycosuria as well as acidosis, though none of the
observations indicates any formation of sugar directly from the fat.
Spontaneous or inevitable downward progress has generally been either
absent or not demonstrable in typical cases of diabetes of even the
worst type. The power of recovering a rather high degree of assimi-
lation at least temporarily has been clearly evident in even the gravest
sort of cases in their incipiency, but never in the extreme stage after
prolonged overfeeding. Success has naturally been easiest with pa-
tients above the age of 30; but with properly appHed treatment,
several cases also of juvenile diabetes have been kept demonstrably
free from downward progress for periods up to 2 years. The defect in
this experience for absolute disproof of the existence of an inherently
or inevitably advancing process in average cases hes not only in the
limited interval of time, but also in the fact that unduly numerous
examples of downward progress have occurred in the present series.
These were attributed to blunders and mismanagement in the appli-
cation of the principle of treatment, which are believed to be plainly
evident in these instances. The hope of continuing this study under
efficient dietetic care has been blocked by war conditions. Therefore
at present a final conclusion is withheld, aside from classing the
"spontaneous" element as at most no more than a minor factor.

RESULTS — PROGNOSIS 595

Final attention must again be called to the limitations inherent in
every dietetic treatment. It affords only rest of a weakened function,
when a stimulus is often needed. Essential progress must take the
direction of supplementing the negative and passive therapy with a
positive and active force. The knowledge of diabetes is advancing
rapidly enough that even the patient whose outlook seems darkest
should take courage to remain aUve in the hope of treatment that can
be called curative.

CHAPTER VIII.
ETIOLOGY AND PATHOLOGY.^

The table of general summary at the opening of Chapter III in-
cludes the etiologic features as far as known. The ratio of 40 males
to 36 females agrees with the accepted view that sex is probably an
indifferent factor. The statistical value of the series depends chiefly
upon the care employed in the study, and is limited by the compara-
tive fewness of the cases and the special standard of selection. Thus
the age incidence shown is worthless, since the choice of severe cases
involved an unnaturally high proportion of young patients. Refer-
ence may be made to the more extensive data of Joslin, Williamson,'
and the older text-books.

The general subject will be considered in the divisions of I, etiology,
II, pathology, and III, chnical application.

I. Etiology.

1. Carbohydrate or Dietary Excess. — This ancient explanation, dat-
ing at least from the Hindu Vedas, is not now seriously considered as
an original cause of diabetes. Even Cantani, the strongest modem
champion of this hypothesis, recognized that some other predisposing
cause must be assumed, because large numbers of normal persons are
guilty of fully as great excesses as those who develop diabetes. This
factor is noted in only a small minority of cases in the above table.
No exact line can be drawn between excess and moderation, but the
conviction has been reached that the previous eating habits of dia-
betics are not noticeably different from those of the general popula-
tion. A few of the patients in this series developed diabetes not-
withstanding an unusually abstemious prior life. Comparisons be-

1 The pathological investigation by one of the authors, outUned here in pre-
liminary form, will be pubUshed in detail elsewhere.

2 Williamson, R. T., Brit. Med. J., 1918, i, 139-141.

596

ETIOLOGY AND PATHOLOGY 597

tween races or classes of society are inconclusive because other in-
fluences than diet undoubtedly enter in. The most tangible evidence
is afforded by experimental animals. " No animal is made diabetic by
carbohydrate or other diet unless it was potentially diabetic before.
Tests with excess of glucose and starch, as also of protein and fat,
for as long as 17 months, have established this fact not only for nor-
mal animals but also for those depancreatized just short of the point
of diabetes. The large margin of safety still present when three-
fourths of the pancreas has been removed shows the impossibility of
damage from carbohydrate with a normal pancreas. This fact is
made still plainer by the observation that the lowering of assimila-
tion from dietary excess in diabetic animals is due to loss of Langer-
hans cells through hydropic degeneration, while the most prolonged
hyperglycemia and glycosuria fail to produce this effect upon the
pancreas of non-diabetic animals.

On the other hand, inasmuch as the aggravating influence of dietary
excess upon diabetes at any stage is well established for both animals
and patients, its role as a possible exciting cause must be recognized.
Le Goff' has shown strikingly the parallelism between the increase of
sugar consumption and of diabetes in the modern civilized world.
Even though the latter increase be chiefly apparent, due merely to
better diagnosis, the raising of the general standard of nutrition and
the development of sedentary Kfe and luxurious habits may well be
expected to make active a certain proportion of diabetic cases which
with lower nutrition and a harder struggle for existence would have
remained latent. Such a conclusion is in Hne with the universal
belief that dietary restriction is an important prophylaxis for those
suspected of predisposition to diabetes by heredity or otherwise.
From the standpoint of prophylaxis, it is to be remembered that sugar
most readily gives rise to glycosuria, and its rapid absorption may
impose a particularly dangerous load upon a weakened assimilative
function, but it is undoubtedly most dangerous in combination with
gluttony; and a regulated mixed diet, rather than carbohydrate
abstinence, is to be recommended for prophylaxis on the same prin-,
ciple as for treatment.

'Le Gofif, Gaz. hdp., 1911, Ixxxi, 5S6-SS8.

598 CHAPTER vin

2. Obesity. — ^Neither the fatness naturally resulting from excessive
eating, nor pathologic obesity can constitute a primary cause of dia-
betes (unless possibly through local fat deposit disturbing the function
of the pancreas) . The supposition that diabetes may for a time be
masked by obesity, through formation of fat from the excess of cir-
culating sugar, is now plainly absurd. The tendency to pathologic
obesity is known to be an internal secretory disorder. Even with a
pituitary or other demonstrated basis for the obesity, it is possible
that changes in the pancreas may at least partly accoimt for the dia-
betes, and more careful pathologic investigations are demanded
rather than speculations. Notice must be taken of the peculiar clini-
cal course of diabetes with h3^ophyseal disease, in that glycosuria
may give way to a high carbohydrate tolerance. It is necessary to
keep clear the definition of diabetes as a deficiency of the internal
secretion of the islands of Langerhans. It is undecided whether
other glands influence the function of the islands, or whether changes
in appetite, food absorption and sugar excretion, and the altered
metabolism of cachexia, merely suppress glycosuria and other usual
symptoms without fundamentally changing the diabetes, the usual
mildness of which is evidenced by the rarity of coma and is appar-
ently confirmed by the pancreatic findings. Broadly speaking, fibrous
and fatty changes in the pancreas may be considered the organic
basis of the obese form of diabetes. Granted this predisposition,
the simple increase of body mass in either physiologic or pathologic
obesity may bring on active diabetic symptoms. The proof is fur-
nished by experiments in which the fattening of animals predisposed
by operation exactly reproduces the development of such diabetes,
and also by the disappearance of s)anptoms and the striking gain in
assimilation when animals and patients alike are reduced in weight.
Since such a high proportion of abnormally obese persons develop
diabetes, the fatty tendency should in itself be taken as a warning.
The dietary control of obesity is the most important prophylaxis
against diabetes in such persons. Also physicians should determine
the glucose tolerance of any noticeably obese patient, by blood as
well as urine analyses, in order to begin treatment in the stage of
hyperglycemia if possible, before glycosuria has ever appeared.

ETIOLOGY AND PATHOLOGY 599

3. Pluriglandular Disorders. — There is no diabetes with a normal
pancreas. This dictum is now accepted even by the vonNoorden
school. As previously pointed out/ diabetes may exist with either
h5^er- or hj^ofunction of other glands. The present series affords
one example (case No. 50) of diabetes with myxedema. Persons with
disorder of one internal secretory organ are doubtless more liable than
normal persons to disturbance in some other organ. Granted a pan-
creatic deficiency, it is conceivable that the increased metabolism of
exophthalmic goitre, and possibly other endocrine intoxications, may
bring on diabetes, though examples are rare. There is at present no
proof that deranged action of other organs can produce either func-
tional or structural abnormahties in the pancreas, and thus serve
as a primary cause of diabetes. The negative results of thyroid
feeding of dogs predisposed by partial pancreatectomy stand against
such an assumption ; but longer experiments and more efficient methods
will be necessary before the problem of glandular interactions can be
satisfactorily solved. The self-evident probability that any organ of
the body is more or less influenced by other organs was grossly dis-
torted and perverted in the polyglandular craze started by Eppinger,
Falta, and Rudinger. These speculations, based largely upon con-
fusion between diabetes and other forms of glycosuria, were promul-
gated with such lack of evidence and have been so completely dis-
credited that only the least informed writers are still guilty of glib
statements concerning antagonism between pancreas, thyroid, ad-
renals, and other glands. Clearer understanding of pancreatic path-
ology will remove much imnecessary confusion. The existence of
other endocrinopathies should never be allowed to confuse the fact
that diabetes is synonymous with pancreatic disease. The thera-
peutic conditions correspond. Hyperthyroidism, for example, as a
possible exciting or aggravating factor in diabetes, should be relieved
by surgical or other means, and benefit to an associated diabetes should
be anticipated. But there is no record of an actual cure of diabetes by
such treatment of a coexisting disorder. Also, pluriglandular disease
with diabetes is the rare exception and not the rule. Not only the
overthrow of the polyglandular doctrine, but also direct experimental

< Allen, F. M., Glycosuria and Diabetes, Chapter XIX.

600 CHAPTER vm

evidence, forbids the extirpation of healthy glands or other mutila-
tions in the attempt to treat diabetes.

4. Constitutional Defects. — This vague notion is mentioned midway
between pluriglandular and hereditary abnormalities, as being more
or less related to both. Minkowski* vigorously denounced this super-
stition. In addition to being too intangible for any use, the concept
of diabetes as a "diathesis" lacks any real support. Defectives of any
sort may naturally show more than the average liability to some other
particular defect. But the majority of diabetics do not appear
constitutionally defective or abnormal. They rather give the im-
pression of an average, often a high type of humanity. Unless there
is some evidence to the contrary, they should be regarded as normal
persons who unfortunately have become afflicted with a definite or-
ganic disease, instead of being branded unjustly with the stigma of
constitutional taint.

5. Heredity. — This holds a traditionally high place in the etiology
of diabetes; but before intelligent judgment is possible, competent
investigators of heredity will have to classify the cases in a fashion
which has not yet been done. Clinically, four provisional groups sug-
gest themselves, as follows:

(a) Cases of Clear-Cut Accidental Pancreatitis, Due Perhaps to Gall
Stones or Any Chance Infection. — Such diabetes might well arise in the
absence of any hereditary history, and — a point of practical impor-
tance— such patients should be capable of producing children free
from any special diabetic tendency.

(&) Familial Diabetes Not Due to True Heredity but to Infection. —
Sj^hiUs is a good example, which has been most strongly emphasized
by Warthin.* The occurrence in successive generations might con-
ceivably be congenital or the result of independent infections, asso-
ciated perhaps with the environment. Three patients of the present
series (Nos. 16, 41, 67) had S3T)hilis, and it is a question whether this
may be viewed as a sufficient cause of their diabetes, without refer-
ence to the family history of diabetes in two of the cases and psychic
disorders in the third; and whether, consequently, there is any danger

'Minkowski, O., Med. Klin., 1911, vii, 1031-1036.

« Warthin, A. S., and Wilson, U. F., Am. J. Med. Sc, 1916, clii, 157-164;
Warthin, A. S., The Harvey Lectures, 1917-18, xiii.

ETIOLOGY AND PATHOLOGY 601

to the children of such patients other than the danger of syphihs.
Most investigators' do not attribute so high an etiologic position to
syphilis as Warthin, but in view of the known pancreatic lesions of
both congenital and acquired syphilis, it could scarcely fail to be
sometimes a cause of diabetes. On the one hand, searching clinical
examinations, Wassermann tests of the spinal fluid as well as of
the blood in suspicious cases, and careful pathologic studies, are
necessary to fix the true etiologic position of syphihs. (In one case
recently seen in military practice, with negative history and nega-
tive Wassermann reaction in the blood, a strongly positive Wasser-
mann test of the ascitic fluid decided the diagnosis.) On the other
hand, the fact should be recognized that most pancreatitis is not
due to syphilis, and this agrees with other evidence that most
diabetes is not due to syphihs.

(c) Numerous Cases of Diabetes without Known Heredity. — It may
be that these are the majority of all cases, just as they constitute
the majority of the present series. There is always the possibility
that an existing diabetic tendency has merely skipped several gen-
erations. Any wide investigation is made almost impossible by two
factors, one the lack of accurate knowledge of even their recent medi-
cal family history on the part of most patients, the other the high
proportion of failures to diagnose diabetes on the part of physicians,
introducing an element of uncertainty into the anamnesis of even
the best informed patient. An occasional patient can estabUsh an
apparently perfect record back to his grandparents, showing a rugged
old age in the majority of his near relatives, and convincing causes of
death in the others. Patient No. 35, for example, came of unusually
sound country stock. The question is made much more prominent
by the occasional instances of diabetes in all or several children of a
family, with parents and ancestors normal as far as known. Foster'
gives an example. A recent patient in this hospital was a 12 year
old country boy, free from diabetic, luetic, or other taint as far as
ascertainable. The family history was not very complete, but con-
tained nothing suspicious except that the mother's father supposedly

' WiUiams, J. R., /. Am. Med. Assn., 1918, Ixx, 365-367.

8 Foster, N. B., Bull. Johns Hopkins Hasp., 1912, xxiii, 54-55.

602 CHAPTER vm

died of tuberculosis (diabetes undiagnosed?). Both parents are alive
and weU, but the record of their children has been as follows: first,
a boy, diabetes discovered at 16, resulted in death at 23; second, a
girl, married, always in perfect health; third, a girl, died of diabetes
at 3; fourth, a boy, died of spinal meningitis at 4 or 5; fifth, a boy,
aged 19, always healthy, now in army; sixth, a girl, died of diabetes at
15 ; seventh, the diabetic boy mentioned. Such remarkable occurrences
raise the question for a large group of diabetics without hereditary
history, as to the possible rSle of innate and of environmental or ac-
quired factors in the causation of their disease.

(d) Cases of Unmistakable Hereditary Character. — In the most pro-
nounced type, there is a high prevalence of diabetes through generation
after generation. Frequently, associated disorders accent the heredi-
tary taint. Although obesity is the best estabUshed of these, Wil-
liams,^ selecting only cases with fairly complete family history, com-
pared 100 diabetics with 100 non-diabetics, and found that arterio-
sclerosis, nephritis, apoplexy, and nervous and mental disorders were
also more common in the ancestors or relatives of the former. If
such associations, on careful examination, prove fundamental, they
will throw valuable Hght upon the nature of the condition. Racial
tendencies also belong here. Not only are savages generally less dis-
posed to diabetes than civilized peoples, but it seems also true that
under similar environmental conditions certain races, as the Jews
and portions of the population of India, are more subject to
diabetes than are other races, as the Japanese. One fact now
seems evident, which is so important for this question that surprise
must be felt that it has never been pointed out before. This is that
even the most typical hereditary diabetes arises, like other diabetes,
on the basis of pancreatitis. True congenital pancreatic hypoplasia,
as described for example by Ghon and Roman,!" jg go rare as to be a
curiosity. Findings of subnormal size or weight of the pancreas
should be judged with reference to general emaciation and inflamma-
tory atrophy. Scarcity of islands has never been established as con-

^ WilUams, J. R., Am. J. Med. Sc, 1917, cUv, 396-406.
!" Ghon, A., and Roman, B., Prag. med. Woch., 1913, xxxviii, 245. A con-
genital deficiency is also mentioned by Hornor, A. A., and Joslin, E. P., Am. J.
Med. Sc, 1918, civ, 47-56.

ETIOLOGY AND PATHOLOGY 603

genital in any case, and as far as known is always the result of de-
generation due either to the cause producing the diabetes or to the
diabetes itself. If this be true, the problem of hereditary diabetes
becomes simply the question why certain families or races are specially
subject to pancreatitis or to a particular form or consequence of it.
Of various possibiHties, three at least have suggestive interest. First,
a purely hereditary explanation might be that the islands are in-
herently defective in function or vitality, so that they either undergo
early senihty or break down under the ordinary strain of Hfe, or suffer
unduly from slight injuries. Arteriosclerosis is one factor to be con-
sidered. The second possibility is a structural pecuHarity predispos-
ing to secondary changes. A clear example might be a duct which
by reason of its form or course is easily blocked. The pancreatitis
and atrophy caused by stasis of secretion is well known in both dogs
and human beings. With reference to Opie's demonstration that
obstruction by a gall stone may result in pancreatitis due to forcing of
bile into the pancreatic ducts, Buntingii pointed out that this is pos-
sible only with a special shape of the ampulla of Vater. It is con-
ceivable that trivial appearing malformations of the duct, head of the
pancreas, or duodenum may conduce to stasis of secretion or circu-
lation, or facilitate the entrance of microorganisms.^^ It may be re-
marked in passing that a pseudohereditary diabetes might be imagin-
able in families or races where occupation or mode of life might be
responsible for malposition, stasis, abnormal intestinal flora, or other
causes of inflammation. A third possibihty is a specific lack of re-
sistance to infection or intoxication. This may be conceived as gen-
eral or local. The latter would mean that the pancreas is abnormally
susceptible to invasion by bacteria, or that the islands are unusually
sensitive to circulating toxins. Certain existing evidence is sugges-
tive for decision among these three possibilities. It would appear,
first, that simple senihty never produces the anatomic picture of dia-
betes; second, that when islands go to pieces from functional over-
strain, they are not invaded or replaced by fibrous tissue; third, that
the form of pancreatitis in hereditary diabetes typicsilly is not that

" Bunting, C. H., Bull. Johns Hopkins Hasp., 1906, xvii, 265-266.
i^Winternitz, M. C, Ibid., 1908, xix, 237-241.

604 CHAPTER vin

which arises from stasis or infection of the ducts. Likewise, jaun-
dice is uncommon in diabetics (Joslin). This leaves the special sus-
ceptibility of the pancreatic tissue or islands to infectious or toxic
injury as a leading possibility; but the evidence is far from sufficient
to warrant anything more than suggestion, and the causes may be
found different in different cases.

The present series includes only 19 known hereditary cases (count-
ing as hereditary all where diabetes occurred in any blood relative),
against 57 without known heredity; i.e., exactly one-fourth were
hereditary to the patients' knowledge. The proportion of Jews was
almost the same; i.e., 18 Jews against 58 of aU other races (chiefly
Americans with ancestry too mixed to distinguish). Of the heredi-
tary cases, there were 6 Jewish against 13 non- Jewish; i.e., about one-
third were Jews. There was no intentional racial selection in admit-
ting patients. Also, the knowledge of their family history certainly
averaged no higher among the Jews than among the others, but it is
noticeable that Jews seem generally better acquainted with diabetes.
In general, the high proportion of Jews and their family histories
support the current view of the racial and hereditary element in
etiology.

If the material can be properly sifted, students of heredity may
perhaps be able to determine to what extent the incidence of diabetes
is governed by MendeHan or other known laws. Aside from its
theoretical interest, the question touches matters of the greatest prac-
tical importance. One of these is prevention, in finding which per-
sons need prophylaxis, and, if the nature of the heritable abnormality
be discovered, in guiding to a more effective means of prevention
than diet. Again, if scientific medicine is to achieve constantly better
treatment and perhaps ultimate cure of all diseases, it must be recog-
nized that a mere cure of heritable diseases like diabetes by no means
removes the heredity, but on the contrary preserves a numerous class,
who formerly died, to transmit their characteristics to a greater ex-
tent than ever before. If such hereditary disease is an indication of
degeneracy in even a single organ, a cure may not prove an un-
mixed blessing sociologically. It can only be repeated that dia-
betics seem often to be persons of high tj^e in their general
characteristics.

ETIOLOGY AND PATHOLOGY 605

6. Nervous Causes. — A nervous etiology of some cases of diabetes,
regarded as a certainty by Naunyn, is supported by the following
seven considerations, (a) Diabetes sometimes runs in the same
families with nervous and mental disorders, (b) Neuropathic in-
dividuals and nervous races are frequently subject to diabetes. Civili-
zation is accused of increasing diabetes by reason of mental and ner-
vous strain, (c) The majority of patients with severe diabetes are
more or less neurotic, (d) Pain, excitement, and any emotional or
psychic disturbances are apt to cause shght glycosuria in normal
persons, and there are numerous reports of the onset of diabetes fol-
lowing such occurrences. Similarly, certain railway statistics are
said to show the highest incidence of diabetes among those , em-
ployees whose work involves greatest danger and strain, (e) Frac-
tures of the skull and spine, and other nerve injuries, often give rise
to glycosuria of variable, generally shght, degree and duration, and
true diabetes has been reported by a number of authors following
such trauma, (f) Existing diabetes is notoriously aggravated by nerve
injury, shock, or strain. Glycosuria occasionally follows operations
upon potentially diabetic dogs, but attempts to imitate clinical con-
ditions adequately in them and in similarly predisposed cats, by t3dng
and the other usual gentle measures, were unsatisfactory, until a cat
imder observation for another purpose by accident escaped from its
cage and was badly mauled by a buUdog, with a resulting aggravation
of the existing diabetes demonstrable for some 2 weeks, (g) Claude
Bernard's puncture of the medulla produces a well known experi-
mental nervous glycosuria; and though Bernard's conception of it as a
transitory diabetes is erroneous, yet in one dog predisposed by re-
moval of three-fourths to four-fifths of the pancreas, it was demon-
strated^' that diabetes was absent before the piqdre and present in
permanent and fatal form after it. This experiment, though isolated,
seems to be positive. Attempts to repeat it have resulted in glycosuria
for no more than a few days, the nervous injuries being either fatal or
else insufficient for permanent diabetes. It is expected that more effec-
tive methods will further demonstrate the potency of nervous irrita-
tion, but it is doubtful if diabetes can ever be produced by nervous

*^ Allen, Glycosuria and Diabetes, p. 775.

606 CHAPTER vrn

agency in an animal with an intact pancreas. Paralytic causes seem
to be excluded by the fact that severing the pancreatic nerves or trans-
planting the pancreas remnant to some other part of the body has no
perceptible effect upon the assimilativ© power. The remarkably di-
lated capillaries of islands occasionally seen in a diabetic pancreas
might suggest a possible vasomotor abnormality, but in partially
depancreatized animals the pancreatic function has appeared widely
independent of the blood supply, unless ligation of vessels were car-
ried to a point resulting in atrophy, thus imitating the possible effects
of arteriosclerosis in a few human cases.

It wiU be noticed that, notwithstanding the multitude of piqdres
and other nerve lesions inflicted upon animals, diabetes has never
resulted unless they were already predisposed. It seems probable
that a similar rule will apply to mankind. Though it is conceivable
that nervous agencies alone may cause diabetes, they probably seldom
are sufficiently powerful or selective to cause it if the pancreas is
normal. Accordingly, they may for the most part be excluded as
primary causes of diabetes and reduced to the rank of secondary
or exciting causes. All the older evidence is susceptible to criticism
in this direction. A causal relationship between diabetes and neu-
roses is no more established by their occurrence in the same families
and individuals than a causal relationship between diabetes and gout
or nephritis. The Japanese furnish an example of a nervously tense
people with an ancient civilization and relative freedom from dia-
betes. Many or most diabetics were not neurotic before the begin-
ning of their diabetes; and so far as causal connection exists, ^the
nervousness is generally the result of the diabetes and the expression
of a badly nourished nervous system, together with anxiety. The
traditional effects of nervous disturbances upon an existing diabetes
are avoided or reduced to a minimum under properly thorough die-
tetic treatment. Real evidence in favor of neurosis or psychic shock or
stress as a cause of diabetes is surprisingly scanty in the present series
of cases. The principal new Hght on this problem is afforded by the
world war, in which it appears that nervous strain, shock, and in-
juries in unparalleled number and variety have occasioned no strik-
ing increase of diabetes. Some cases must necessarily arise, as in
civil Hfe. The question of the importance of the nervous factor is

ETIOLOGY AND PATHOLOGY 607

at present answerable only from the older statistics, which seem to
indicate that it somewhat increases the incidence of diabetes; in other
words, that this exciting cause perhaps suffices to develop some cases
which otherwise would have remained latent.

7. Trauma. — ^This topic necessarily overlaps and is partly synony-
mous with the preceding. The strict criterion of traumatic diabetes
heretofore has been absence of glycosuria before the injury and its
presence within a reasonably short time thereafter. This is incom-
plete cKnical evidence, for doubtless in many such cases hyperglycemia
already existed. Scientifically conclusive proof could be furnished
only by pathologic examination. It is a justified prediction that the
pancreas in almost any case of tramnatic diabetes is the seat of abnor-
malities antedating the trauma. Experiments with direct and indirect
injuries of the pancreas in animals, and the clinical knowledge con-
cerning acute pancreatitis, practically exclude the possibiUty of any
immediate production of diabetes by direct pancreatic traimia; either
the damage will faU short of this, or it wiU cause death rather promptly.
It is conceivable, however, that acute injury of a previously normal
pancreas may inaugurate a process which will later result in diabetes.
Such cases have never yet been demonstrated and must necessarily
be rare. No clear-cut example of traumatic diabetes has been seen
at this hospital. The recent war has given the death blow to
trauma as an important cause of diabetes. For practical purposes,
the best foimded view-point is that trauma, shock, nervous injuries,
etc., bring on diabetes only when the pancreas is already diseased.
Autopsies upon all possible cases of traumatic diabetes, especially if
death occurred shortly after injury, are highly important in this
connection. Medicolegally and otherwise, the status of tramna is
like that of other exciting causes, in that it seemingly gives rise to
some cases which otherwise might not have become active. Whether
diabetes might have been anticipated without such an exciting cause
could be judged to some extent by a qualified pathologist, but not in-
fallibly. Compensation to the injured individual is not thus invali-
dated, since there is no doubt that any exciting cause may at least
hasten the onset of an impending diabetes or aggravate an. eixifeting
diabetes. i ' *

608 CHAPTER vm

8. Infection and Inflammation. — The most advanced views of the
infectious etiology of diabetes were expressed recently by Woodyatt"
as follows:

"Diabetes mellitus, a name now given by clinicians to any case in which as
the chief incident — or as one of several incidents — there occurs from natural
causes a diminution of the endocrine function of the pancireas sufficient to cause
the symptom diabetes. The factors which determine such diminutions are
infections of the pancreas, the term implying an interaction between a suscep-
tible tissue and a suitable pathogenic germ. So called diabetic predispositions con-
sist in inherited susceptibilities to certain types of infection. Well known varia-
tions in the clinical course of diabetes in the same case at different times and in
different cases are not wholly ascribable to variations in diet, etc., but often to
infectious moments. Concurrence of other diseases as Basedow's, dyspituitarism,
myocarditis, arteriosclerosis, etc., with diabetes, are not due to 'correlation of
ductless glands,' nor to metabolic disturbances secondary to diabetes, but to
simultaneous infections in different tissues." Prophylaxis is held to consist in
preventing diabetogenous infections (tonsillitis, sinusitis, pyorrhea, parotitis,
cholecystitis, ulcer, prostatitis) rather than in dietary restrictions. "These
views are based on the literature, an analysis of 100 chnical cases with aid of
D. E. Abbott, the character and frequency of pancreas lesions in 538 animal
inoculations with different strains of streptococcus group by E. C. Rosenow,
clinical improvements following treatment of foci of infection in certain cases,
previous views of Rumpf, Lepine and others, general development of knowledge
concerning relation of foci of infection to visceral diseases (Billings, Rosenow,
Irons, and others), knowledge of the selective affinity of certain strains for cer-
tain tissues (Rosenow)." Woody att has also placed strong emphasis upon the
occasional cases of acute diabetes accompanying acute infectious disease, in
which apparently normal carbohydrate assimilation is regained after recovery
from the infection.

The above may stand as the clearest expression of the Rosenow
school concerning diabetes, related to their corresponding doctrines
concerning other diseases. Notwithstanding an active following,
this contention in general is not at present regarded as estabhshed by
the majority of the medical profession. For diabetes in particular,
importance is assigned to focal and other infections by J. R. Wil-
liams, while Joslin in his wide experience, and Greeley^^ in an analysis

1* Woodyatt, R. T., Abstract of Proceedings of Seventh Annual Meeting of the
Americam Society for the Advancement of Clinical Investigation, 1915, 25-28.
^ Greeley, H. P., Wisconsin Med. J., 1915-16, xiv, 464-468.

ETIOLOGY AND PATHOLOGY 609

of the large material of Hodgson's sanitarium, were unable to find
evidence that such infections are more prevalent among diabetics
than among other hospital patients, or that they are a determining
factor in the chnical course. The interpretation of transitory dia-
betes accompanying an acute infection is necessarily ambiguous,
since the latter might be a primary or merely an exciting cause, and
the assimilation might subsequently appear normal even though the
pancreas were reduced considerably in mass or function. Proof
of the frequency 9f pancreatic lesions in experimental septicemia wiU
be a valuable contribution, but such experiments cannot in themselves
be decisive unless they produce either diabetes or a marked and per-
manent lowering of sugar tolerance. The above writers have cour-
ageously recognized that the hypothesis of an infectious etiology of
all cases of diabetes must be extended to various other metabolic
disorders. The particularly close relation of diabetes and obesity
must hold also here. While it is not impossible that obesity may
yet be numbered among the infectious diseases, such a bold concep-
tion must appear tpday as prophecy rather than proof. The un-
certainties in the whole subject of diabetes are such that tangible
evidence is the chief need.

The one tangible and outstanding fact is the frequency with which
pancreatitis has been described by all authors of all shades of opinion
who have made accurate microscopic observations in diabetes. The
present pathologic study has given an unexpectedly sweeping cor-
roboration of this lesson from the earUer work. It is possible to set
up a general dictum, "without pancreatitis, no diabetes," and chal-
lenge pathologists to produce exceptions. A diabetic pancreas in
which careful search fails to reveal more or less evidence of present
or past inflammation is at least a great rarity, and, if ever found,
will merely illustrate the remarkable completeness of organic
recovery sometimes possible after acute inflammation even of a degree
sufficient to produce diabetes. The principal stumbling-block has been
the apparent discrepancy between structure and function, as found
in the presence of diabetes with seemingly insufficient anatomic altera-
tions, and the absence of diabetes with more extreme visible change;
and this disagreement persists even with distinctions between inter-
lobular and interacinar forms of pancreatitis, and with comparisons

610 CHAPTER vin

limited to destruction of islands rather than of total parenchyma.
Discussion must partly be deferred to the subsequent section on pa-
thology; but much of the uncertainty necessarily connected with
cUnical conditions is cleared away by consideration of animal experi-
ments, divisible into the following four groups.

(a) When the duct and perhaps part of the blood supply of a pan-
creatic remnant are occluded, gradual atrophy brings on the well
known Sandmeyer diabetes, as late as 13 months after operation in
one of that author's cases. Such diabetes has never been produced
with the whole pancreas m situ, even when the ducts have been in-
jected with paraflSn by Claude Bernard and others, or recently with
alcohol by Auer and Kleiner." The extreme degeneration and
sclerosis finally resulting were shown in the pathologic examinations
of Sandmeyer, J. H. Pratt, and Auer and Kleiner. Nevertheless,
diabetes has not been observed unless two-thirds or more of the
gland has first been removed (or, rarely, destroyed by gangrene).
The reason evidently is that indigestion, emaciation, and cachexia
are in progress at the same time, and prevent the famihar diabetic
sjTnptoms even when the destruction of islands has reached a point
at which the animal must be classed as potentially diabetic. With
the entire pancreas present, thtese other disturbances will cause death
before frank diabetes develops; but removal of most of the gland
causes the internal secretory deficiency to become manifest earlier in
proportion as the pancreatic remnant is smaller.

(b) After simple partial pancreatectomy leaving the remnant with.
natural duct drainage, the tissue generally remains soft, lobulated,
and normal, except for a narrow zone of fibrosis adjoining the area
of amputation. More or less hypertrophy occurs sometimes; other-
wise conditions are found unchanged even after several years. The
nutrition and assimilative power are correspondingly maintained
unless the remnant is so small that the animal is potentially diabetic,
in which case dietary and metabolic influences may cause functional
and structural decay of the islands, without inflammation or fibrosis
and without alterations in the acinar tissue.

1^ Auer, J., and Kleiner, I. S., Proc. Soc. Exp. Biol, and Med., 1916-17, xiv,
151-153.

ETIOLOGY AND PATHOLOGY 611

(c) Sometimes more or less fibrosis takes place in a pancreas
remnant, presumably as the result of undue trauma in the operation.
Upon tliis hint, it was found possible to produce diabetes with con-
siderably larger remnants than usual, by setting up inflammation by
crushing between the fingers. The course of the fibrosis follow-
ing acute injury varies. Sometimes the process apparently halts,
so that no further impairment of structure or function is evident in
rather extended observations. In other cases the sclerosis continues,
so that diabetes develops after several weeks or months, and the pan-
creas remnant is found atrophic, sometimes almost as extremely as
after occlusion of the duct.

(d) As a better means of inducing aseptic inflammation, rubber-
covered clamps were applied to cut off the blood supply for 20 min-
utes to 2 hours continuously. Diabetes results more easily in propor-'
tion as the pancreas remnant is smaller, but has been produced with
fully a third of the pancreas present. Part or the whole of the

. imcinate process is the most convenient remnant for this purpose.
Shorter periods of clamping are used at first; if diabetes does not re-
sult, gradually longer stasis can be applied in later operations without
death from fat necrosis. Apparently only technical obstacles pre-
vent producing diabetes with the entire pancreas present. This would
have much theoretical interest, but the success actually achieved is
sufficient to estabhsh the principle. Incidentally, the pancreatic
gangHa withstand anemia for as long as 2 hours, so that the hope of
observing the effects of the loss of the intrinsic nerve supply has been
disappointed. The after-etfect of this acute experimental inflamma-
tion reproduces strikingly the pancreatic pictures seen with clinical
diabetes. Various grades of chronic fibrosis are found; but the
most interesting result is a pancreas which is soft, lobulated, and
normal appearing in gross, and which microscopically is charac-
terized by scarcity of island tissue, without corresponding destruction
•of acini, and with visible evidences of pancreatitis apparently alto-
gether too slight to account for the condition. Either the islands
are injured more easily and profoundly than the acini, or their power
of recovery is less. The trivial cHnical disturbance in the dogs even
during the early period of most intense pancreatitis is also remark-
able, but it could not be safely inferred that human patients would

612 CHAPTER VIII

be equally little affected. It is therefore of interest that Whipple"
found acute inflammation of the pancreas precisely similar to the ex-
perimental form in 6 out of 230 unselected autopsies, most often with
pneumonia and a smaller proportion with other infections, and stated:
"These cases were all under careful observation in the wards of the
Johns Hopkins Hospital, and gave no s5Tnptoms of pancreatic disease."
Though the two columns of infections in the General Summary table
(beginniag of Chapter HI) may at first glance seem imposing, a classi-
fication of the 76 cases of this series will show something like the fol-
lowing four groups:

(a) 23 cases characterized by more or less numerous infections,
the causal relationship of which to the diabetes must be purely specu-
lative, without any definite indications. These are cases Nos. 1, 4,
6, 8, 9, 11, 13, 14, 15, 19, 20, 21, 29, 31, 32, 38, 42, 44, 48, 49, 53,
63, 72.

(b) 29 cases not only lacking any suggestive infectious etiology of
the diabetes, but rather exceptionally free from infections in general.
These are cases Nos. 2, 7, 10, 12, 18, 22, 25, 34, 35, 39, 45, 46, 47,
50, 51, 52, 54, 55, 57, 58, 64, 65, 66, 68, 70, 71, 73, 74, 75.

(c) 9 cases in which an infection stands in suggestive relation with
the outbreak of diabetes. Patient No. 3 not only had "colitis" 5
years before admission, but, just before the first diabetic symptoms,
suffered appendicitis and appendectomy, followed by phlebitis ap-
parently indicating septicemia. Patient No. 5 at the beginning of
his diabetes had symptoms which may have represented acute pan-
creatitis. No. 24 gave a clear-cut history of obstructive jaundice,
without evidence of gall stones oo: biliary infection, followed within a
year by the gradual onset of diabetes. The child No. 26 had some
unknown disturbance which caused vomiting, followed immediately
by diabetes. The suspicious condition in another child, No. 28, was
merely fever of unknown origin; the subsequent slight choreiform
movements do not prove that it was poliomyelitis, and it might
have been pancreatitis. In No. 36, the beginning of diabetes is
significantly related with general sepsis. No. 37 had nothing but an
alveolar abscess, then an ordinary cold; diabetes promptly followed.

"Whipple, G. H., Bull. Johns Hopkins Bosp., 1907, xviii, 391-396.

ETIOLOGY AND PATHOLOGY 613

No. 40 was admitted for pneumonia; he had apparently been a well
man before, and his apparently complete recovery from the diabetes
suggests pneumococcus pancreatitis as the probable cause. The
young boy No. 76 had only otitis media, indicated by earache and
fever. Diabetes quickly followed, and the only further evidence of
pancreatic involvement is that digestive upsets have since occurred
from sKght causes.

(d) IS cases in which at least a possibility of connection exists be-
tween diabetes and pancreatic injury produced by some infection
acquired many years previously. Three of these (Nos. 16, 41, 67)
are cases of syphilis. No. 17 had a serious combination of pneu-
monia and empyema 20 years before admission, and a later history of
indigestion. No. 23 had suffered from "bloody dysentery" 14 years
previously. No. 27 had had mumps with orchitis at the age of 18, a
pancreatic involvement being imaginable; there was also "jaundice"
at the age of 20. No. 30 had passed through some ordinary infections,
and gave a significant history of "nervous indigestion" and pale feces
for years past. No. 33 twice suffered from acute nephritis following
colds. The pancreas is certainly as susceptible to infection as the
kidney, and there was a history of indigestion. In No. 43, this com-
bination of sepsis and nephritis, with subsequent diabetes, is especially
striking. No. 56 had inflamed cervical glands in childhood, and was
also subject to gastrointestinal attacks with fever of unknown origin.
No. 59 gave a history of biliousness, nausea, and vomiting through-
out childhood. No. 60 had had "gastric fever" in 1896. No. 61 in
childhood had suffered from intractable diarrhea; subsequently he
had typical rheumatism; and as the infectious origin of his cardio-
renal disease is not doubted, the same may be assimied as the cause
of pancreatitis. No. 62 gave an, unintelligible description of some
childhood trouble possibly related to her diabetes. In No. 69,
sepsis may be thought of as a possible cause.

The elements of personal judgment and clinical uncertainty are
illustrated here as necessarily in all such inquiries. It is to be recog-
nized that groups (a) and (6) comprise 52 cases, or over 68 per cent
of the series. That is, this large majority shows no perceptible rela-
tion between known infections 'and diabetes. The relations sug-
gested in groups (c) and (d) are purely a matter of interpretation and

614 CHAPTER vni

carry no demonstration in any instance. The connection supposed in
group {d) between events so many years apart might easily and
sometimes doubtless rightly be considered imaginary.

The most definite group, (c), is open to quite different interpre-
tations, by reason of the well known facts that diabetics are specially
liable to infections and that existing or latent diabetes is aggravated
by infection. Thus, patient No. 40 might have had some preexisting
diabetic tendency; the latent diabetes may have been awakened by
the pnevunonic infection and subsided again with the subsidence of
the latter. Zealous advocates of infection might choose to change
cases Nos. 6 and 38 from group {a) to (c). But there is here no evi-
dence of anything but pneimionia in persons already mildly diabetic;
thus, patient No. 6 considered herself well before the pneumonia,
when there was no knowledge of diabetes; she continues to consider
herself well now, when it is known that glycosuria is constantly
present. Patient No. 57 was included in group (J), because measles
at the age of 8 was the only illness known before his diabetes. The
accidental fact that he studied medicine afforded the sole informa- .
tion that glycosuria was present then, 8 years before the supposed
onset of diabetes. Except for this, it would have appeared that
repeated tonsillitis and then furunculosis were followed by diabetes,
and the case might have been placed in group (c) on suspicion of
staphylococcus pancreatitis. In patient No. 41, diabetes was first
discovered in connection with a cold and sore throat, as in some of '
the cases in group (c) ; but in him the more probable cause of diabetes
is syphilis. It is probable that minor abnormalities, as of the teeth
and lymph glands (see again General Summary, Chapter III) are no
more common in diabetics than in 'others, unless as the result of the
diabetes; and an etiologic position has never been demonstrated for
them in any case. In the absence of other infections, some might
lay stress upon caries and pyorrhea in suCh a case as No. 67 ; but here *
syphilis is known to exist. AU the cKnical conditions are therefore
confusing, and the only trustworthy guide is the pathology. This
compels recognition of the fact that, unless these diabetics are dif-
ferent from the large series ' covered by the present microscopic
study and from the many others in the Mterature, the basis of the
disease in all of them is pancreatitis. The existence of pancreatic

ETIOLOGY AND PATHOLOGY 615

inflammation, and the search for its cause, is thus extended to all
four groups alike. The cause ordinarily to be supposed is bacterial;
but a connection with any other general or focal infection is clinically
discoverable at best in only a minority of cases, and even in them is
subject to many doubts and mistakes.

The basis of belief in the inflammatory origin of diabetes is there-
fore essentially a generalization from the classical studies of diabetic
pathology, with experiments and deductions to clear away some
apparent inconsistencies and confusion. The view of Woodyatt and
others of the Rosenow school, concerning the status of focal infec-
tions, specific relations of bacteria to organs, etc., is a distinctly new
suggestion, concerning which the above observations do not decide.
This contention in diabetes is on the same basis as in a variety of
other diseases, and must stand or fall as the general evidence may
determine.

II. Pathology.

Since the former review of this subject,^' papers have appeared by
Koch," supporting the archaic notion that the islands are merely
degenerate and functionless portions of the parenchjmaa, and by
Major,'"', dealing with a comparative study of the pancreas in 35
non-diabetic and 13 diabetic necropsies.

The pathologic changes of the pancreas in diabetes are divisible
into those causing the diabetes and those resulting from the diabetes.

A. Changes Causing Diabetes.

For general purposes, details of fibrous, fatty, hyaline, and other
alterations may be ignored, and all cases grouped roughly in three
classes, as follows.

1. Cases of extensive loss of parenchyma, involving islands and
acini alike, and in the most extreme instances comparable to the
Sandmeyer diabetes of dogs. The earliest pancreatic lesions described
by Cawley and others were naturally of this class.

^' Allen, Glycosuria and Diabetes, Chapter XXI.

"Koch, K., Virchows Arch. path. Anat., 1913, ccxi, 321-330.

2" Major, R. H., J. Med. Research, 1914, xxxi, 313-330.

616 CHAPTER vin

2. Cases of selective injury of islands. There is never much
destruction of islands without some involvement of the acinar tissue,
and all gradations between this and the first group are met, but the
best instances, notably of fibrous and hyaline change, well justify
Opie's use of them as the basis of the insular hypothesis.

Under this same heading may be mentioned also certain peculiar
pictures, described early by Weichselbaum and StangP^ and recently
by Wilhams and Dresbach,^^ but not heretofore correlated as stages of
a special process. They may in fact not represent a distinct and pro-
gressive sequence, but comparison between different cases and be-
tween different portions of the same pancreas frequently reveals the
following graded examples. In the seemingly incipient form, the
island appears sometimes congested, frequently hypertrophic, and
perhaps irregular in structure, but the essential feature is the striking
pyknosis of certain nuclei, with the cytoplasm about them often only
a narrow band. Even at this stage, sHght fibrosis or at least a few
round cells are present. Through successive degrees, this condition
seems to pass over into what Weichselbaum and Stangl called atrophy
of the islands, in which condition they are small, more or less fibrous,
and characterized predominantly by the shrivelled cells with pyknotic
nuclei and scanty cytoplasm. These pictures, though common, are
doubtful in interpretation. The change is distinguishable from typi-
cal hydropic degeneration; for though pyknosis of nuclei is a feature
of the latter, it is plainly subsequent to the vacuolation of the cyto-
plasm. Shrunken cells may be present in the same island with
hydropic cells, but apparently never become hydropic themselves,
perhaps because they are no longer functional. Weichselbaum and
Stangl considered the atrophic islands not diagnostic of diabetes, be-
cause found in some non-diabetic cases.' In 1911, Weichselbaum
again mentioned this atrophy, in which the island cells resemble
l)nmphocytes, and this time considered it probably a result of hydropic
degeneration, therefore diabetic. This picture is very rare in experi-
mental diabetes, but what is probably a true reproduction of it has
finally been observed in a few diabetic animals. Here also the

^'^ Weichselbaum and Stangl, BibHograpKy of Chapter 1.

22 Williams, J. R.. and Dresbach, M., Am. J. Med. Sc, 1917, cliii, 65-78.

ETIOLOGY AND PATHOLOGY 617

shrinkage of island cells is accompanied by round-cell infiltration,
and the change is probably inflammatory in origin.

Its presence raises a suspicion of diabetes; and even if the latter be
absent, the reason might be only that the change is not yet sufficiently
advanced or general. Widespread " atrophy" of islands is diagnostic
of diabetes, generally of the severest form. Islands showing this
change in advanced degree are certainly functionless, because they
are often present in large numbers in cases with scarcely any food
tolerance. The finding of such "atrophy" after widely different
dietetic management, i. e. in flagrant diabetes with no food restric-
tion whatever, and after the traditional protein-fat diet as in
Weichselbaum and Stangl's cases, and also in cases kept symptom-
free by prolonged rigid imdernutrition, furnishes partial proof, first,
that it is not of dietary origin, and second, that it is permanent and
irremediable under any form of treatment now known.

3. Cases in which the visible abnormalities in both islands and
acini seem too slight for a rational explanation of the diabetes. Some
of these have given rise to the behef that diabetes may exist with a
histologically normal pancreas. Some examples have been cases of
very rapid course in young persons, formerly supposed to represent
the extreme of severity, and therefore responsible for considerable
confusion in the past. Autopsies of such cases in their incipiency are
rare and therefore will be specially valuable whenever obtainable.
From some examples of early death in coma, however, it is possible
to infer that diabetes may begin with a pancreas showing only slight
fibrous or round cell invasion and containing an apparent abundance
of normal looking islands. One difficulty in forming quantitative
judgments is that the amount of pancreatic or island tissue necessary
to prevent diabetes in man is not known. Comparison with animals
is unreKable, since these vary widely and irregularly, from the cat at
one extreme, which becomes diabetic with about a fifth of the pan-
creas remaining, to the pig, in which a tiny fragment of pancreas
prevents both diabetes and cachexia. The monkey approximately
resembles the dog in requiring removal of seven-eighths to nine-tenths
of the pancreas for diabetes. Man is probably to be reckoned among
the most highly susceptible species, but the few reports of resection
of the human pancreas do not suffice for decision, partly because of

618 CHAPTER vin

inexact estimation of the portion removed or left, and partly because
the pancreas in such cases is diseased. Careful surgical, medical, and
pathologic studies of such patients in the future wUl possess obvious
importance. The best information at present seems to be afforded
by the case of Ghon and Roman," of a boy dying at the age of 14, with
idiocy, status lymphaticus, and other abnormalities, including a
congenital pancreatic deficiency, apparently the result of failure of
development of the dorsal pancreatic anlage, so that only the portion
formed by the ventral anlage was present. This roughly rectangular
plate of tissue adjoining the duodenum measured in its greatest
dimensions 7.4 cm. in length, 4.5 cm. in width, and 2 cm. in thickness.

Microscopically, "the changes consisted on the one hand in a focally occurring
increase of the interstitial tissue, in which here and there also small roimd cell
infiltrations were observable, and on the other hand in an everywhere observable
injury of the Langerhans cell islands. In comparison with the pancreas of a boy
of the same age dead of scarlet fever, studied for a control, the Langerhans cell
groups of our case showed not only increase of the intrainsular connective tissue,
but also the change which Weichselbaum has described as hydropic degeneration.
The hydropic degeneration change was mostly demonstrated only in its incipient
stages, but we saw also many islands, which following Weichselbaum we could
designate as atrophic."

The boy was physically well developed, and the existing diabetes
therefore probably of recent origin. The authors are doubtless jus-
tified in attributing its onset to the sUght pancreatitis rather than
to the simple metabolic strain of growth and puberty. There is a
further possible question whether the abnormalities in the body else-
where had any influence, and even whether the inherent functional
capacity of the islands was normal. On the whole, however, it ap-
pears that this considerable piece of pancreas was barely suflScient for
metaboHsm, and that diabetes ensued when it was only slightly in-
jured by inflammation. This interpretation agrees with other scanty
evidence that man is rather highly susceptible to diabetes, and that
the "margin of safety" in the human pancreas is not so wide as in
most experimental animals.

In addition to anatomic destruction, the existence of a functional
incapacity of the island cells must be assumed, and is demonstrated,
even without excessive labor of counting and measuring islands, by

ETIOLOGY ANT) PATHOLOGY 619

the following five facts: (a) Autopsy comparisons show that diabetes
often exists in cases where island tissue is widely and unmistakably
more abundant than in other cases without diabetes. (6) The ana-
tomic deficiency of islands is generally demonstrated only at death
from diabetes, after a course of months or years, during which pan-
creatitis or hydropic degeneration or both have been in progress;
and it must be assumed therefore that islands were more plentiful
at the beginning of the diabetes, (c) As illustrated by certain cases in
the present series and others,^' the most intense, even "total" dia-
betes may exist, as demonstrated by the dextrose-nitrogen ratio and
the respiratory quotient, and yet fasting may bring the condition
under control and a tolerance amounting sometimes to hundreds of
grams of carbohydrate may rapidly be recovered. Such patients
formerly met early death in coma, supposedly because of the hopeless
severity of their disease, and perplexity concerning the pathology
was created when they were found sometimes to possess a consider-
able abundance of apparently normal islands. It is now evident
that the recovery of assimilation under fasting would be impossible
if islands were not thus present; and these findings, formerly a
ground of argument against the insular hypothesis, actually serve to
support it. In the preliminary publications, it was deduced from this
fact alone that the deficiency of the islands must be at least partly
functional, (d) When some cells of the diabetic islands show hy-
dropic degeneration, a functional insufficiency must be assumed also
in the cells which appear normal. The accepted interpretation of the
hydropic change in both man and animals implies that the cells are
overtaxed functionally while they still appear normal, and the visible
vacuolation follows, (e) Though it is possible to find animal speci-
mens in which the exhaustion is universal, this condition has never
been observed in man. Even when the diabetes is not only maximal
by the usual tests, but furthermore so severe that it cannot be con-
trolled by fasting, the islands contain not only exhausted cells but also
others which appear structurally normal. The latter sort are fre-
quently so mmierous that a functional disabiHty must be admitted.

^ AUen, F. M., and Du Bois, E. F., Arch. Int. Med., 1916, xvu, 1010-1059. •

620 CHAPTER VIII

B. Changes Due to Diabetes.

The years 1900 and 1901 are epoch making in the microscopic
pathology of diabetes, for in them appeared not only Opie's study of
changes causing the disease, but also the first description by Weich-
selbaum and StangP^ of the hydropic degeneration, which later has
proved to be a result of the diabetes. Those authors described the
process as a vacuolation and liquefaction.

"There appear in the protoplasm of single or several epithelial cells of the
islands sniall vacuoles, or, more objectively expressed, small, round spots, within
which the protoplasm, which otherwise ordinarily shows a very close and fine
granulation and stains lightly but distinctly with eosin, appears entirely trans-
parent and colorless. These so called vacuoles then become confluent, and in the
cell body are seen now only isolated granules and threads, which barely stain
with eosin, while all other parts of the cell body appear entirely homogeneous,
transparent and colorless, till finally also the individual granules and threads
disappear, and the nucleus is now surrounded only by a perfectly transparent and
colorless cytoplasm. Whether the latter in the condition just described is to be
regarded as fluid, or has merely become extremely thin and transparent, we wish
to leave undecided. But as the change begins with a vacuolation and a break-
down of the protoplasm, and furthermore often the chromatin of the nucleus
becomes indistinct and finally a complete dissolution of the latter follows, we
have chosen the designation, liquefaction. In such islands, the remaining, not
yet liquefied epithelial cells show an exceedingly thin, delicate, but still not homo-
geneous and transparent protoplasm. It is therefore not improbable that a
thinning of the protoplasm precedes the above described vacuolation and
liquefaction."

These observations, beginning with 18 cases of diabetes, were ex-
tended so that in 1911 Weichselbaum was able to report 183 diabetic
necropsies, with "a, still larger number" of non-diabetic controls.
Of the diabetic cases, 53 per cent showed hydropic degeneration or
atrophy, 43 per cent fibrous, and 28 per cent hyaline changes. These
were described, as was inevitable under the circumstances and in the
absence of animal experiments, together as the three principal lesions
causing diabetes. The recognition of the hydropic change was facili-
tated by the fact that the diabetic material was mostly from severe
cases with termination in coma, and by the care taken for freshness

^^ For bibliography see Chapter I, also Allen, Glycosuria and Diabetes, Chap-
ter XXI.

ETIOLOGY AND PATHOLOGY 621

and fixation of tissue with a view to applying special stains. The
broad plan of the work also contributed notably to its success, a
careful study of the normal histology having been first made by
Stangl, later the development was studied in the fetus and infant
by Weichselbaum and Kyrle, and finally the pathology was closely
investigated in the largest series of diabetic and non-diabetic cases on
record. The admirable manner in which the research thus planned
was carried out makes it a classic. Both the descriptions and illus-
trations show clearly and convincingly the exact appearances en-
countered in the study of any long series of t)^ical cases of severe dia-
betes. The discussion is also worthy of such a foundation, the
necessity of examining many sections from different parts of the pan-
creas, the non-specificity of hemorrhages in the islands, the pictures
indicative of regeneration and hyperplasia, the consideration of quan-
titative changes, the answers to opponents of the insular hypothesis,
and the etiologic suggestions, being still worthy of notice.

The investigation carried on at Harvard, 1909 to 1912, developed an
improved form of experimental diabetes, in which hydropic degenera-
tion of islands was found to occur. Descriptions and photographs
were published in the former monograph.^^ The vacuolation was
proved to be specific to diabetes and to run parallel to the clinical
course, and was interpreted as exhaustion due to functional over^
strain. Professor F. B. Mallory, with whose aid and advice the
microscopic study was made, first suggested that the visible exhaus-
tion of cells might be the result of the diabetes.

Reference was made in that publication to the work of Lane and
Bensley, who proved by differential staining that the islands contain
two types of cells. What they called the a cells are few in num-
ber, while the fi cells make up the main mass of the island. The
different affinity of the fine (presumably secretory) granules of these
cells for dyes distinguishes them from each other and (along with
mitochondrial and other characteristics) also from acinar, duct,
centroacinar, a'nd imperfectly differentiated island cells.

Homans^" in 1912, using Bensley's stains, demonstrated the loss of
granules of the /3 cells, so that they came to resemble duct cells,

^^ AUen, Glycosuria and Diabetes, 1913.

^^Homans, -i^Proc. Roy.Soc. London, Series B, 1912, Ixxxvi, 73-87; /. Med.
Research, 1914, xxx, 49-68; 1915-16, xxxiii, 1-51.

622 CHAPTER VIII

in dogs made diabetic by removal of all the pancreas except a small
fragment at the tip of the uncinate process. He was inclined to in-
terpret it as a specific exhaustion due to functional overactivity, but
hesitated to regard the r61e of the islands in carbohydrate metabolism
as positively proved. In 1914 he pubhshed a fuller investigation,
altogether independent of that of Allen, showing that in cats mild
diabetes is accompanied by thinning and later complete loss of gran-
ules from the ;8 cells, while the nuclei and mitochondria remain
normal, and more severe diabetes is marked by degeneration and dis-
appearance especially of the fi cells, though a granules may
also remain in only a few cells. In 1915 he reported similar observa-
tions in dogs, indicating uniform preservation of a cells while ;8 cells
degenerated, the possible new formation of small islands composed
only of a cells, and the production of the hydropic process by carbo-
hydrate food, the sequence being defined as activity, exhaustion, and
degeneration. An illustration was also given of an exactly similar
vacuolation of the fi cells in a human diabetic, confirming Weichsel-
baimaand Stangl.

Hydropic degeneration has also been described in the above men-
tioned case of Ghon and Roman," and in an interesting and important
instance of spontaneous diabetes in a dog studied by Krumbhaar.^'

Martin,^* under the direction of H. M. Evans at Johns Hopkins,
tested various pure dyes of the group used by Bensley, and determined
that the best for the purpose is a combination of ethyl violet with
either orange G or azofuchsin. The latter may be particularly recom-
mended as an improvement upon Bensley's original stains, in that it is
easier and more reliable in apphcation and gives more vivid and dis-
tinct pictures. This work was continued in connection with the dia-
betic investigation in this Institute. The existence of the two kinds
of granules in normal island cells was confirmed. The work being
incomplete, Martin did not reach a conclusion whether the granules
were confined strictly to different cells. He suspected that there
might be gradations, and that two sorts of granules might be present
sometimes in the same cell, but owing to possible overlapping of cells
and other elements of doubt, he did not feel justified in opposing

" Krumbhaar, E. B., /. Exp. Med., 1916, xxiv, 361-365.
28 Martin, W. B., Anat. Rec., 191S, ix, 475^81.

ETIOLOGY AND PATHOLOGY 623

Bensley's carefully formed opinion that the two cell types are wholly
distinct. Romans' discovery that only the /3 cells are subject to the
characteristic exhaustion and degeneration was corroborated, and this
fact favors Bensley's view of the independence of the two types.
Often the a cells persist with if anything heavier than normal granu-
lation among the swollen and vacuolated p cells, as described by
Homans. This investigation was applied to dogs in which the metab-
ohsm and clinical condition had been carefully studied, in the hope
of gaining information of the function of the a cells, but no definite
relation between them and any phase of the diabetic disturbance was
observed. Even the persistence of a cells in dogs showing a "total"
D : N ratio could not prove them unconcerned in carbohydrate metab-
ohsm, since there is the possibility of a functional disabiHty, such as
must sometimes be assumed for the /3 cells, and also of functional
interrelations normally between the two types of cells. In the
extreme stages of experimental diabetes, vacuolation occurs in the
sniall ducts and ceU-cords, suggesting a real or attempted internal
secretory function in them, though this is uncertain.

The vital and' differential staining methods open important fields of
research. Knowledge of the normal and the comparative histology
of the pancreas is by no means complete. Though the essential in-
dependence of the islands is established by the work of Bensley and
by their specific degeneration in diabetes, the frequency and extent
of new formation of both islands and acini from ducts, the behavior
of the islands in inflammation, regeneration, etc., and the exact
border Hne between normal and pathologic processes, may be
mentioned as unsettled problems. In diabetes and other patho-
logic states, it is still sometimes impossible to distinguish between
acinar and island cells; the problem of regeneration and hyper-
plasia of island tissue has practical as well as theoretical bearings;
and the function and relations of the several types of island cells,
together with the duct and centroacinar cells, will be learned only by
stud3dng abnormal, as well as normal organs. A point of particular
interest was whether the special stains would furnish the long sought
infalHble anatomic diagnosis of diabetes. There was a chance that
the islands which cause confusion in some diabetic cases might prove
to be composed of a. cells only; also that sparseness of granulation

624 CHAPTER vni

might reveal diabetes in some instances where ordinary stains showed
normal appearances. These conditions may in fact occur to some
extent; but on the whole it is found, in agreement with conclusions
expressed by Homans in conversation, that the special stains do not
remove the difl&culties of diagnosis. They furthermore are rather
difi&cult and laborious in appKcation, they demand a freshness of
tissue and perfection of fixation seldom attainable in human autopsies,
and even under ideal conditions in pathologic material they often
fail to give the differentiation desired.

It is fortunate for practical convenience that routine methods care-
fully applied are sufficient. More or less can be learned from ordi-
nary pathologic specimens in Zenker or formaldehyde solution, and
neutral formaldehyde or Miiller-formol mixtures are preferred by
some. Instead of the usual 5 per cent acetic Zenker, the fixative of
choice in the present work has been either a plain solution of 2.5
per cent potassium bichromate and 5 per cent mercuric chloride, or
the same solution with addition of 1 or 2 per cent acetic acid just
before using. Lane and Bensley have found that stronger acidity
tends to dissolve out the specfic island granules. The most im-
portant consideration for the study of hydropic degeneration is the
freshness of the tissue. The autopsy should be performed immedi-
ately after death if possible, and the first step in it should be the re-
moval and weighing of the pancreas, followed by immediate fixation
of the pancreas specimens. It is advisable to take specimens from
different parts of the gland in separate bottles. The procedure here
has unconsciously imitated Weichselbaum and Stangl in taking them
in three sets, from the head, body, and tail respectively. It is also
desirable to take two kinds of specimens from each location: one,
pieces of ordinary size, for the purpose of examining the nimiber of
islands and the general pathology; the other, tiny bits of tissue, only
a few millimeters in dimensions for the sake of the quickest possible
penetration of the fixative for the study of the cytology of the islands
with either special or routine stains. For the latter the combina-
tion of eosin and either hematoxyhn or methylene blue has been satis-
factory in the present work. The fixation of other specimens in
formaldehyde for fat or in absolute alcohol for glycogen stains, and
other special measures, are of course added when desired. Persons

ETIOLOGY AND PATHOLOGY 625

contemplating an investigation, will do well to begin with animals, in
which the diabetic change is plainest, and then to examine some
human specimens showing it in typical advanced form, after which
they will be better equipped to judge more doubtful material.

Information concerning hydropic degeneration may be summarized
under six headings, as respects its description, nature, cause, mechan-
ism, consequences, and significance.

1. Description. — ^Histologically, the process begins with a thinning
of the fine granules, supposedly of internal secretion, shown in the
island cells by the Bensley methods, or a paling and clearing of the
finely granular cytoplasm seen with ordinary stains. The finest
routine preparations probably reveal the change almost as early and
delicately as the special dyes. The progress of the vacuolation or loss
of granules is as described by Weichselbaum and Stangl and by
Romans. The swelling of the individual cells, seemingly by imbibi-
tion of fluid, is apt to be more prominent in the dog and especially
the cat than in other species, such as man, monkey, and raccoon, but
occurs in all. In the most extreme degree, the islands composed of
swollen empty cells somewhat resemble adipose tissue; Homans com-
pares the network of cell membranes to a coarse meshed sieve; or the
exhausted islands may seem to blaze out against the dark back-
ground of the acinar tissue like snowballs or hydrangeas in full bloom.
Differences between species and between individual examples in
the same species are governed largely (though perhaps not solely)
by the acuteness of the process, giving both a more intense
swelling and a greater number of simultaneously exhausted cells
than when the change is slower. The alteration in the nucleus
seems to be strictly secondary. An apparently normal nucleus
can sometimes be seen naked, after the cell membrane has
burst. The nucleus does not, as might be implied by Weichselbaum
and Stangl's description, simply dissolve; but ordinarily at some,
generally an advanced, stage of vacuolation of the cytoplasm, it
becomes markedly dense and shrunken, and this pyknosis is one of
the prominent features of the process. The shrivelled nucleus then
dissolves, and is the last part of the cell to disappear. The observa-
tion of Weichselbaum and Stangl, that the hydropic change first begins
in occasional cells, while most cells in the same island and all cells in

626 CHAPTER vin

many islands still appear normal, holds for all species. Many /3 cells
remain free from vacuolation even when many others have com-
pletely disintegrated. In the more advanced stages, recourse to the
differential stains may be necessary to determine whether the re-
mainder are the usual a cells, or |8 cells persisting with slight alteration
or none. The order of precedence in which cells are affected is not
governed by their position at the center or periphery of the island,
or any obvious relation to the blood supply, or other known rules.
The loss of cells is not replaced by fibrous tissue; neither, except in
the most acute stage, are visible gaps left; but the acinar tissue
crowds in on all sides, whether by new formation of acini or other-
wise is unknown, and the reduced island remains as a compact group
of cells, until finally it may consist only of a barely distinguishable
clump of a cells and more or less framework, or may disappear with-
out a recognizable trace.

2. Nature. — There is nothing to oppose Weichselbaum and Stangl's
assumption that the vacuolation represents essentially water. The
ordinary appearances, in addition to Sudan stains, suffice to rule out
fat. Tests for protein and salts have not been made. Most observ-
ers are immediately impressed with the similarity to the Armanni or
Ehrlich change in certain cells of the renal tubules. Glycogen has
not been demonstrable by Best's carmine in the vacuolated islands.
The cause or nature of the renal picture calls for investigation. It has
been commonly accepted as "glycogenic infiltration" because of
EhrHch's demonstration of the presence of glycogen in diabetes.
The renal and pancreatic phenomena are not on a par, since the
former may be found in various conditions while the latter is specific
to diabetes. The truest resemblance is probably to the empty cells
found in the adrenal medulla when nervous or other stimuli exhaust
the fine granules which supposedly represent the precursor of epi-
nephrine stored in the chromaffin tissue. Bensley in conversation sug-
gested the possibihty that the Langerhans vacuoles may contain the
internal secretion in too great dilution for deposition in granules.

3. Cause. — Experimentally, the hydropic change can be shown to be
specific to diabetes. It does not follow pancreatic operations unless
diabetes is produced. Dogs made potentially diabetic by such opera-
tions can be kept even for years, and the preservation of their islands

ETIOLOGY AND PATHOLOGY 627

can be demonstrated not only microscopically but also by the un-
changed or increased food tolerance. But after any interval, early or
late, the characteristic change can be produced by adding to the diet
any kind of food beyond the assimilation, or by anything else that
brings on active diabetic symptoms. Its independence of digestion is
shown by its occurrence in fasting animals after removal of sufficient
pancreatic tissue to cause active diabetes during fasting. It is like-
wise independent of other pathologic processes, such as give rise to
diabetes. For example, hydropic degeneration does not give rise to
fibrosis, neither does it ever result from simple fibrosis of any island,
no matter how extreme. But when diabetes occurs, the presence of
fibrous or other changes does not prevent the typical hydropic proc-
ess, which in fact is generally found side by side with the fibrous
and hyaline changes in the t3^e of cases in which the latter have been
most emphasized by Opie and others. A point of particular practical
importance is that simple prolonged hyperglycemia, without glyco-
suria, regularly and definitely produces this change in diabetic ani-
mals; it is merely slower than with the more intense condition of
hyperglycemia plus glycosuria. A slight degree of vacuolation may
also be found in transitory diabetes, not only with glycosuria, but
even when the animals for some days following operation show merely
a considerable hyperglycemia on carbohydrate diet. The change
may be demonstrated in a tiny bit of pancreas removed at this time
without affecting the condition. Subsequently it may be impossible
to bring on diabetes by any amount of starch and sugar feeding, and
though temporary hyperglycemia may result, the island cells are not
vacuolated. It must be concluded that the condition following
operation was a genuine mild diabetes, even if evidenced only by
hyperglycemia; and that subsidence of inflammation and functional
and structural restoration and perhaps hypertrophy in the pancreas
remnant resulted in a final cure.

4. Mechanism. — Experiments have been conducted to show the
possible r61e of humoral and nervous agencies. Of the former, it
might be supposed that the blood sugar is predominant, and that
hyperglycemia per se is the stimulus to the islands. The evidence is
against such an assumption. Vacuolation of the islands does not
follow even the most prolonged hyperglycemia in normal animals,

628 CHAPTER vm

one example being the experiment described in the former mono-
graph by one of the authors, in which glycosuria was maintained by
glucose injections in a cat during the greater part of 17 months, with-
out producing vacuolation in the pancreatic cells or any other accom-
paniments of diabetes. Adrenalin and other forms of glycosuria like-
wise do not cause this change. Phloridzin has given useful results.
Phloridzin poisoning, continued even for many months, does not
cause hydropic degeneration; the unchanged sugar tolerance thereafter
would be sufficient proof, even without the microscopic examina-
tions. But when dogs are made severely diabetic by removal of all
but a small fragment of pancreas, and, beginning even before opera-
tion, receive phloridzin in small doses so as not to produce fatal
acidosis or intoxication and yet keep the blood sugar continuously
at an actually subnormal level, hydropic degeneration occurs in fully
t3rpical fashion. Of nervous influences, it was shown in the former
monograph that the Bernard puncture ordinarily causes no vacuo-
lation in the islands, but in the single predisposed dog in which true
diabetes followed the puncture, the characteristic hydropic change
occurred. Romans,^* producing hyperglycemia and glycosuria by 7 to
10 hours faradic stimulation of the splanchnic nerves in animals
possessing an entire pancreas or only a half or a fifth of it, was un-
able to demonstrate positive alterations in the islands. Even poten-
tially diabetic animals, however, fail to show vacuolation from hyper-
glycemia due to glucose injections within such an interval. The
questionable swelling and diminished granulation of the cells men-
tioned by Romans may possibly indicate a positive effect, which was
prevented from becoming inanifest only by the time limitations. A
paralytic injury seems to be excluded by both denervation and graft
experiments. The best procedure for this purpose is to leave a small
remnant about the lesser duct to aid digestion, and to transplant the
button of duodeniun bearing the main duct along with the entire
uncinate process beneath the skin of the abdomen, preserving the
blood supply of the graft through the inferior pancreaticoduodenal
vessels, and removing all the rest of the pancreas. Division of this
pedicle some weeks later isolates the graft from all intra-abdominal
connections. Removal of successive portions from both the duodenal
remnant and the subcutaneous graft then shows that both diabetes

ETIOLOGY AND PATHOLOGY 629

and island changes are absent until the total remaining pancreatic
tissue is reduced to the degree required to produce diabetes in an
ordinary operation; food then shows the usual influence, and the
usual hydropic changes occur in both the duodenal remnant and the
subcutaneous graft. The graft of course acquires a nerve supply,
presumably vasomotor, along with the blood supply from the sub-
cutaneous tissue. Also the intrapancreatic ganglia survive, and no
experiments have succeeded in eliminating the possibility of their
regulating action*. What is proved is that both the normal internal
secretion and the hydropic process go on apparently unchanged in the
absence of any possible specific stimulus or control from centers out-
side the pancreas. It may be conjectured that the regulation of the
function of the islands, as probably of endocrine organs in general, is
both nervous and humoral. Both experimental and clinical evidence
suggests the possible influence of nervous stimuh, at least for harm.
The humoral agency is proved; but it does not lie in hyperglycemia,
which is merely a symptom of active diabetes. A special hormone
is conceivable. But as mass action is an explanation of growing im-
portance for physiological regulations, it may be that variations in the
concentration of the internal secretion (whether this be combined
with food substances such as sugar, or free) in the blood serve to govern
the formation and discharge of this substance by the cells.

5. Consequences. — The hydropic degeneration results in numerical
atrophy and finally almost complete disappearance of the islands of
Langerhans. Weichselbaum and Stangl did not distinguish between
this clear-cut process and the more recondite "atrophy" in which the
island cells resemble lymphocytes. It seems probable that in the
earlier stages compensatory regeneration and hyperplasia also occur.
This view is supported clinically by the marked recovery of tolerance ■
often possible at such a stage, developmentally by the formation
of islands from ducts, which Laguesse and Bensley proved to con-
tinue in postembryonic life, and pathologically by the rather fre-
quent finding of enlarged, seemingly hyperplastic islands, and of
others that appear as if newly formed. Duct-Uke strands of cells,
and small, compact, generally oval islands, unUke those usually seen
normally and sometimes looking definitely like proliferations from
ducts, have been mentioned by Homans and are a familiar observa-

630 CHAPTER vrtr

tion in diabetic animals. In man such islands seem to be as a rule
spherical, since their cut section is approximately round. It has
seemed fitting descriptively to refer to them as the "morula" type of
islands. They are not merely contracted islands with empty capil-
laries, but conform to Bensley's description of secondarily developed
islands, and in their most typical form they are pushed in between
the acini as morula-hke masses of cells without capsule or the ordi-
nary capillary and trabecular framework. They are strikingly fre-
quent in some cases of diabetes, being sometimes ahnost the only
type of island present. The finding of a considerable proportion of
such islands may create a suspicion of diabetes; but, even granting
the interpretation of them as "young" islands, it is not surprising
that they may be found in the absence of diabetes, since regenera-
tion need not be Kmited to the diabetic pancreas, and may iti fact
sometimes be the means of preventing diabetes. The islands of this
type may suffer hydropic change and be lost like the others. Whether
they are functionally equal to the ordinary islands, whether the cells
are commonly paler and more subject to exhaustion and degeneration,
are only speculative suggestions at present. Regeneration, even if
a reality, fails in the later stages. Apart from the uncertainties of this
question, two important facts are fully established. On the anatomi-
cal side, the deficit in number and mass of islands demonstrated in
diabetes by Opie, Weichselbaum, Heiberg, and others, as far as it is
not due to destructive processes causing the diabetes, is the result of
the diabetes itself through hydropic degeneration; and in many cases,
especially some of the worst type in young persons, this latter process
is responsible for the loss of most of the islands. On the physiological
side, this phenomenon explains clearly the progressive loss of tolerance
caused by improper diet, and enforces the lesson of the difficulty or
impossibility of repairing the damage.

6. Significance. — ^Active diabetes must first be present in order for
the hydropic change to occur. In the partially depancreatized ani-
mal, a small fragment of pancreas evidently attempts unsuccessfully
to carry the whole metabolic burden. In human patients, the islands
present are apparently likewise stimulated to meet a demand beyond
their capacity. Presumably the cells respond with an actual or at-
tempted increase of secretory activity for a longer or shorter time

ETIOLOGY AND PATHOLOGY 631

while appearing morphologically normal. At length secretion is dis-
charged more rapidly that it can be formed, so that the normal fine
granulation becomes more sparse and is replaced by vacuolation.
Finally nuclear degeneration and complete disintegration of the cell
result. This interpretation is so clearly suggested by the anatomic
appearances, and so plainly confirmed by the feeding experiments,
that there has been full agreement on the point among recent investi-
gators. For this reason, the term "exhaustion" has come to be used
as synonymous with vacuolation.

Physiologically, this phenomenon may be compared to the dis-
charge of the acinar cells of the pancreas by secretin. There is a
difference, in that secretin or other hormones have never been known
to cause destruction of cells and actual disappearance of the tissue
upon which they act. Whether the difference Hes in intensity or
duration of stimulation or in pecuharities of the cells is unknown.
A further distinction is that an internal secretory function is here
concerned, and the process is a clear-cut example of anatomic break-
down of an endocrine organ by functional overstrain. A strikingly
clear relation between function and structure is thus shown, and the
conception of diabetes as the overstrain of a metaboUc function, long
probable on clinical grounds, is strongly confirmed. The experi-
ments with partially depancreatized animals are so simple and definite
that this biologically important phenomenon is made easy to study.

III. Clinical Application.

This includes practical deductions concerning the etiology, anatomic
diagnosis, and treatment of diabetes.

A. Clinical Etiology.

The etiology of diabetes will probably become fairly clear as soon
as the pathology of the pancreas is adequately studied. Notwith-
standing all the past work, the pancreas remains a neglected and
little known organ from the simple anatomic-pathologic standpoint, as
may easily be seen from the cursory remarks on it in text-books.
The normal variations must first be better known. Occasional atj^pi-
cal appearances were noted by Opie and others, and Oertel and

632 CHAPTER vin

Anderson^' are the most recent authors to interpret these as indicating
a natural sequence of degeneration and regeneration, though a ques-
tion of their true normality is raised by the statement that they
occur chiefly after middle Ufe. A comprehensive investigation must
be comparative. The present war, for example, may afford unusual
opportunity for extensive observations on the pancreas of supposedly
healthy individuals; but even if a high proportion show pecuharities,
the question whether these are normal phenomena or reactions to
morbid influences can be answered only by comparison, with a series
of animal species. The same mihtary opportunity might be utilized
to obtaiQ a series of specimens from the more primitive races of man.
It might then be possible to judge whether the erect posture, civilized
habits, or other factors render man specially lia,ble to pancreatic
disorders and hence to diabetes.

An elementary fact, which seemingly should have attracted notice
before, is that the pancreas is one of the most frequently diseased
organs in the body. There is even ground to question whether a
strictly normal pancreas may not appear as the exception rather than
the rule in miscellaneous autopsies. Doubtless the percentage of
abnormaUties is lower in the young and rises with age, just as the
incidence of diabetes is known to increase with age. The clinical
diagnosis is missed in the great majority of cases, because of the
deep situation of the organ hindering physical examination, the ab-
sence or slightness of digestive disturbance, and the fact that only
the most violent forms of pancreatitis give the symptoms recognized
as characteristic, while in milder or more chronic cases the local or
general signs are indefinite or imperceptible, or if present are ob-
scured by other morbid conditions. With due regard for nervous,
hereditary, and other contributing influences, the central problem of
the practical etiology of diabetes is the cause of the pancreatitis which
may be predicated in every case, as a rule with no exceptions yet
demonstrated.

Three forms of injury are distinguishable. One is the well known
inflammation produced by bile or obstructed pancreatic secretion, the
immediate harmful agency being chemical but the cause back of it

^'Oertel, H., and Anderson, C. M., Royal Victoria Hospital (Montreal), Scien-
tific Reports, 1916, Series B, 163-173.

ETIOLOGY AND PATHOLOGY 633

generally bacterial.'" Another is damage by bacterial products, lo-
cally or from a distance. There can be no doubt of the occasional
r61e of organisms, as those of syphilis, lying in the parenchyma, or of
colon or other bacteria in the ducts. Also any pathogens circulating
in the blood might perhaps attack either the capillaries or the epi-
thehum. Injury by soluble toxins from remote foci seems more
vague and dubious. Such a possibiHty is supported by threefold
evidence: (a) familiar lesions in viscera, including the pancreas,
from extensive burns and other severe intoxications; (&) the fre-
quent hyaline and rare amyloid changes, often affecting particu-
larly the islands, and best explained as of toxic origin; (c) the easily
demonstrable impairment of assimilation which so often accompanies
even sHght infections. The injury seems to be direct, since it is
difl&cult to imagine any important metaboUc alteration from a trivial
cold, for example. It also appears to be functional, since rigid con-
trol of symptoms by dietary restriction during the attack ordinarily
permits recovery of the full tolerance thereafter, while any permanent
lowering resulting when symptoms are not thus controlled is readUy
explainable by hydropic degeneration. It is possible, however, to
conceive of intoxication causing first functional deterioration and
then structural decay, in the form of pyknosis of nuclei, atrophy of
cells, and fibrosis of capillaries and islands..

Miscellaneous localized infections found in a certain proportion of
diabetics may be variously interpreted as pure accidents such as
befall nimierous non-diabetics, or as a result of the lowered resist-
ance characteristic of diabetes, or as a source of infection or intoxi-
cation directly causing the diabetes. It is probable that each of these
three possibilities is sometimes correct. The demonstrable fact of
damage to the islands of Langerhans by infectious disturbances, and

'" Concerning pancreatitis from bile, see Halsted, W. S., Bull. Johns Hopkins
Hosp., 1901, xii, 179-182; Opie, E. L., Ibid., 182-188; Am. J. Med. Sc, 1901, cxxi,
27-43; Flexner, S., J. Exp. Med., 1906, viii, 167-177.

Concerning pancreatitis from injection of bacteria, acids, alkalies, and other
irritants, see Flexner, Johns Hopkins Hosp. Rep., 1900, ix, 743-771; Flexner and
Eearce, Univ. Penn. Med. Bull., 1901-02, xiv, 193-202. Glycosuria is frequent
with acute pancreatitis, according to Flexner's experiments and the clinical ex-
psrience of Emerson, Bull. Johns Hopkins Hosp., 1908, xix, 95-96.

634 CHAPTER vni

the need and benefit of clearing up discoverable foci in any case, do
not prove, however, that the focus or organism in question is the
original cause of the diabetes. Removal of infectious foci responsible
for continuous or recurrent intoxication naturally prevents the in-
jury due to such intoxication. The clearing up of slighter foci, as
dental caries or pyorrhea, in the absence of perceptible systemic
symptoms, though advisable on general principles, seldom has much
influence upon the assimilation. The rule with all foci is that their
treatment gives relief from a distinct aggravating influence, but
never a cure of the diabetes or a subsequent course different from
cases without known foci. It is reasonably certain that a diabetes
due exclusively to gall stones from typhoid or colon bacillus infection,
or to pancreatitis from S)rphiHs, pneumonia, or mumps, would show
precisely the usual aggravation from a staphylococcus middle ear
abscess or a streptococcus tonsUUtis. Therefore conclusions should
not too lightly be drawn that such a focus is the primary cause of the
diabetes, either as a source of circulating toxin or as a portal of entry
of organisms.

This problem can only be solved by more careful investigation of
the incidence and causes of pancreatitis. '^ Whipple's study, already
mentioned," consisted in examinations of the pancreas in 230 un-
selected autopsies. Of these, 105 appeared normal; the others showed
more or less pancreatitis, classified in five groups. The 6 cases of
acute diffuse pancreatitis, occurring with pneimionia or other infec-
tions without recognizable symptoms, were mentioned above in con-
nection with the similar inflammation which in animals is proved to
be productive of diabetes. The three other classes of acute changes
were 41 cases of focal necrosis, apparently not serious in degree, 5
cases of fat necrosis, and 7 cases of acute hemorrhagic pancreatitis.
The remaining group of chronic pancreatitis embraced the majority of
cases. FeiUng ^^ expresses the opinion that mmnps is the commonest
cause of pancreatitis in childhood. He cites authors who have diag-

'* Cf. Egdahl, A., A Review of One Hundred and Five Reported Cases of Acute
Pancreatitis, with Special Reference to Etiology; with Report of Two Cases,
Bull. Johns Hopkms Hasp., 1907, xviii, 130-136: McCrae, T., Acute Pancreatitis
in Tjrphoid Fever, Assn. Am. Phys., May 7, 1918.

'2 Feiling, A., Quart. J. Med., 1914r-lS, viii, 263-264.

ETIOLOGY AND PATHOLOGY 635

nosed pancreatitis in respectively 4 out of 60 and 5 out of 33 cases
of mumps. Autopsies on cases of mumps are rare, and it is reason-
able to suppose that pancreatitis escapes notice more often than it
is recognized. There have, however, been only a few reports of
glycosuria or diabetes with mumps. The hyperglycemia or glycosuria
frequently reported in connection with other infections is sometimes
diabetic, more often doubtful in character.'^

The occurrence of acute pancreatitis without diagnostic symptoms is
highly suggestive in regard to the etiology of diabetes. It is conceiv-
able that the condition occurs either with general infections or in-
dependently, and that diabetes may result immediately or after
various intervals. In delayed cases, the acute inflammation may
render the organ susceptible to later injuries, or time may be re-
quired for the damaged islands to break down under metabolic strain.
Thus, in children particularly, it is imaginable that an infection occa-
sioning slight or imperceptible S3anptoms may leave the patient ap-
parently as well as before, yet really with pancreatic deficiency which
months or years later, under the burden of growth, becomes manifest
as diabetes, seemingly of acute onset. The possibiKty was mentioned
that with diabetic heredity such inflaimnations may be either more
frequent, or, by reason of an inherently subnormal functional power
of the organ, more serious in their consequences; and accordingly there
will be special interest in examinations of the pancreas of both the
non-diabetic and the -diabetic members of diabetic families. The
hardness of the pancreas so often noted by surgeons in operations is
hkewise of interest, though internists and pathologists dispute the
rehability of such observations. While the commonest origin of
chronic pancreatitis may be gall stones and biliary infections, there is
room for inquiry concerning other prolonged causes, and also to
what extent acute inflammations are responsible for progressive later
changes, through obstruction of circulation or secretion by fibrous
tissue.

However uncertain the symptoms, there is reason to believe that
pancreatitis of any marked degree is not a matter of indifference for
the general health; and the pathologic facts warrant the prediction

^ Allen, Glycosuria and Diabetes, pp. 564 and 798.

636 CHAPTER vni

that it will some day receive more attention as a cause of acute and
chronic illness. When an adequate diagnostic method is developed,
the new domain of pancreatitis will largely be carved out from the
diagnoses which today are essentially expressions of ignorance, e.g.
"dyspepsia," "nervous indigestion," "neurasthenia," "gastroenter-
itis," "autointoxication," "biliousness," "catarrhal jaundice," as well
as other indefinite abdominal troubles or vague general impairment
of health. Particularly with regard to "catarrhal jaundice," it is
worth while to question how often the stasis of bile is due to swelling
of the head of the pancreas, or, if due to primary bile duct infection,
how often this spreads to the pancreas, and whether in all such cases
thought should not be directed to the pancreas as the organ chiefly
in danger. Clinical observations (cf . table. Chapter III) support the
view that diabetes and indigestion generally do not occur together,
partly because, as Opie showed, the type of pancreatitis is often dif-
ferent, and also doubtless because the malnutrition of pancreatic
indigestion opposes the development of active diabetes.

The frequency of pancreatic inflammation may give reason for
surprise that the damaged organ is so often able to prevent diabetes,
but removes the principal element of mystery from the cases that
occur.

B. Anatomic Diagnosis.

Three chief difi&culties have hindered the study of pancreatic
pathology.

First, the organ is subject to incidental changes which may efface
its ordinary characteristics. Thus, OerteP* describes cellular atrophy
and collapse of structure to such an extent that islands and acini
are not distinguishable. These changes, which have nothing to do
with diabetes, but are purely the expression of pancreatic involution
from cachexia or other cause, are necessarily an obstacle in diagnosis,
especially important because terminal cachexia is so common in dia-
betes. Here the islands may show appearances like Weichselbaum's
atrophy, with shrunken cells and pyknotic nuclei, without proving
any specific disease in them. It is necessary also to be critical of

'^Oertel, H., Royal Victoria Hospital {Montreal), Scientific Reports, 1916,
Series B, 155-162.

ETIOLOGY AND PATHOLOGY 637

reports of the gross weight of the pancreas, since this may be found
low without indicating anything more than emptiness of the organ
and general malnutrition.

Second, cytological observations have not been considered in the
purpose or in the. preparation of material of most researches in the
past. Autopsy specimens are seldom ideal, often for reasons outside
the power of the pathologist. In the main, however, attention has
been centered upon the grosser structural disorganization, and the
carelessness of pathologists regarding finer cellular changes is respon-
sible for their overlooking the vacuolation accurately described and
pictured by Weichselbaum and Stangl. It is furthermore important,
in estimating dearth of islands, to recognize th* pseudo-islands which
occur in some cases, probably from proliferation of duct cells, and
which lack both the structure and function of true islands.

Third, the clinical grouping of cases has been misleading. Inher-
ently mild diabetes has been classed as severe merely because of
acetonuria or perhaps an unnecessary death in coma. Maximal
severity has been attributed to certain cases on the ground of their
rapid course and early fatal termination. Since such patients when
given the opportunity by proper treatment often manifest a surpris-
ingly high assimilative power, the finding of numerous islands in their
pancreas is now seen to be in strict accord with the insular theory,
instead of inimical to it as formerly supposed. With a truer clinical
classification, and with treatment preventing a large proportion of
early unnecessary deaths, pathologists will find the inicroscopic diag-
nosis much simpler. On the other hand, the clinical statement that
diabetes was absent need not be accepted as infallible. Generally it
means only absence of glycosuria. Tests of the blood sugar and glu-
cose tolerance have seldom been made, and even these may be viti-
ated by cachexia or other disturbances. Weichselbaima records one
instance in which the pathologic findings pointed to diabetes, which
was not clinically evident during the final iUness in the hospital,
but careful inquiry of the relatives elicited a history of typical diabetic
symptoms previously. In most diseases the pathologist corrects the
clinician, not vice versa; and this will be increasingly true of diabetes
as the morbid anatomy is better understood.

638 CHAPTER VIII

The diagnostic import of the island exhaustion resulting from dia-
betes, and of the lesions causing diabetes, may be summarized as
follows:

1 . Hydropic Degeneration. — It is necessary to define the signifi-
cance of the presence and absence of this change.

Its Presence. — Vacuolation of cells is an appearance which patholo-
gists are likely to view with suspicion as an accidental or unreHable
phenomenon. Forttmately the islands of Langerhans are little sub-
ject to non-specific vacuolation. Fry'^ mentions vacuolation and
degeneration of the islands in a case of myxedema. The bare possi-
bility of masked diabetes must be considered; or, as vacuolation of
the adrenals is similarly mentioned, it is conceivable that the change
in the islands may have been fatty. Extensive examination of mis-
cellaneous autopsy specimens has thus far confirmed Weichselbaum's
conclusion in favor of the specificity of the true hydropic alteration.
Careful study is still needed to decide whether actual fluid accumu-
lation ever takes place in the island cells from any cause other than
diabetes, and whether fatty or other changes ever simulate the real
exhaustion. The most frequent cause of uncertainty is imperfect
preservation of tissue. Shrinkage, as from formaldehyde, small
breaks in the sections, and other artefacts may be confusing. Especi-
ally, with only a little delay in fixation, the dehcate menlbranes of
exhausted cells may break down first of all; and with later autopsies
blurring and fragmentation of the islands may make pictures hard
to interpret. Under these circumstances simple pallor of island cells,
and the finding of naked nuclei, is suggestive but not conclusive.
With abundant islands present, there may then be justified hesita-
tion between two extreme judgments; one, complete absence of dia-
betes, with perhaps nothing wrong but a trivial pancreatitis; the
other, diabetes of the most intense rapid ty^Q with early death in
coma. Diagnosis is sometimes demanded not only from poorly
fixed tissue but also from single sUdes, whereas search through all
portions of the pancreas is required by the fact that certain areas
sometimes reveal pictures not seen in the others. It seems safe to
say that the typical picture of vacuolation in some cells and pyknotic

35 Fry, H. J. B., Quart. J. Med., 1914-15, viii, 276-299.

ETIOLOGY AND PATHOLOGY 639

nuclei and degeneration in others is absolutely diagnostic of diabetes.
Furthermore, if in satisfactorily prepared tissue an observer familiar
with this process finds a single island cell which is unmistakably
swollen and vacuolated, with a nucleus (generally normal) surrounded
by a halo of clarified cytoplasm inclosed within a distinct cell mem-
brane, in sharp contrast to the other normal appearing island cells,
the existence of diabetes is estabhshed. Only, the warning against
accidental appearances more or less closely imitating the true pic-
ture must here be emphasized. As the sign is one of active diabetes,
the clinical record regularly agrees; but if any exception is found,
the cHnical diagnosis should be subjected to fully as close scrutiny
as the pathologic diagnosis.

Its Absence. — In animals the hydropic change is a fairly reUable
and delicate index of diabetes, beginning with slight vacuolation of a
few cells in the early mild stage, and advancing parallel with the
duration and severity. It appeared puzzling that a considerable pro-
portion of human cases, surpassing in both these respects many of
the animals, show entire absence of visible exhaustion; yet the ex-
planation is simple. In the strictest sense, the hydropic degeneration
is an expression not of diabetes but of cellular dissolution due to
diabetes. It is unknown at what point repair becomes impossible;
but in animal experiments a cell evidently persists only a few days
in its terminal stage of extreme vacuolation and swelling. Under
sharp dietary restriction, gradual recovery seems to be possible even
at this stage, apparently corresponding to the marked transformation
and gain of tolerance in some human cases on fasting. Otherwise,
cells and islands break down and are permanently lost, as already
explained. Human cases seldom progress as rapidly as the experi-
mental diabetes of animals, in which the destruction of islands may
be practically complete within a few weeks or months, as proved
anatomically and by the inability to become sugar-free on fasting.
The human cases are more likely to last months and years, and even
in the worst forms to retain enough island tissue to enable control
by fasting. Accordingly, the visible degeneration could not be so
striking in the human pancreas as in animals unless the clinical prog-
ress were as rapid. Moreover, the intensity of clinical symptoms
is not a sole criterion of the anatomic effects. Not only may a dog

640 CHAPTER vin

with a 2.8 or lower D: N quotient show more rapid and extensive
island destruction than a man with a 3.65 :1 ratio, but the differences
between human patients are still greater. It is well known that
cases with similar hyperglycemia, glycosuria, and acidosis differ
widely in progressiveness, such differences being most familiar be-
tween elderly and youthful patients, but sometimes equally prom-
inent between different cases at the same age. Specific differences
in the susceptibihty of the island cells to anatomic breakdown
from functional overstrain must be recognized. Therefore it is
impossible to establish any rule as to the proportion of cases in
which hydropic changes wiU be foimd. It can only be said that
they, are invariably present when the intensity and the duration of
the diabetes are sufl&cient. They are practically always present in
typical coma, though when this foUows only a short period of intense
symptoms, they may sometimes be surprisingly slight and hard to
demonstrate. Specimens from severe cases of diabetes treated by
the old methods show them in the majority of instances. They are
less frequent in proportion as the diabetes is milder or the treatment
more efficient. The previous statement that persistent hypergly-
cemia without glycosuria causes degeneration of islands is a deduction
as applied to human cases. The evidence for it is that diabetic ani-
mals under these circinnstances show gradual loss of tolerance, and
slight hydropic changes are demonstrable in their islands. Human
patients show a similar injury of assimilation, which is sometimes so
slow that it may appear doubtful but is nevertheless real; but the
anatomic process has not as yet been observed in them under these
conditions. Such a gradual loss, probably no more than the disin-
tegration of an occasional scattered cell, though real, will necessarily
be seldom convincingly visible. Diminished frequency of hydropic
degeneration should be the accompaniment and proof of improved
treatment.

In brief, the presence of hydropic degeneration may be held to
establish a positive diagnosis of diabetes, but its absence is not
proof that diabetes is absent.

2. Lesions Causing Diabetes. — ^AU pathologic researches on the
subject have agreed concerning the occurrence of pancreatitis, and
notably of fibrous, hyaline, fatty, pigmentary, malignant, or other

ETIOLOGY AND PATHOLOGY 641

changes affecting the islands, in a variety of conditions without posi-
tive diagnostic significance, but on the whole more frequently and ex-
tensively in diabetic than in non-diabetic cases. In the nature of
things, it has been impossible to establish any uniform rule for the
diagnosis of diabetes from such observations, for several obvious
reasons. First, valid judgment of the extent of island destruction
requires unusually painstaking study, because of the differences even
between closely adjacent areas of the normal pancreas, as shown by
Bensley, and still more so in pathologic material. Second, some
allowances must be made for functional influences and differences, as
mentioned previously. Third, the pathologist cannot be expected to
estimate concomitant clinical conditions. The characteristic active
symptoms of diabetes may be absent with emaciation from anorexia,
impaired food absorption, or any form of cachexia, when the pancre-
atic destruction is such as would certainly bring on these symptoms
in a patient otherwise healthy. The condition is entirely similar
to the apparent absence of diabetes in cachectic dogs possessing only
insignificant atrophic remnants of pancreas. This is doubtless the
chief explanation of the usual lack of diabetic symptoms with pan-
creatic cancer. In the main, the inabiUty to draw a sharp pathologic
line between diabetes and non-diabetes merely expresses the fact
that no such hne exists. There are all gradations between normal
and diabetic, with or without demonstrable impairment of food
assimilation. With a certain allowance for functional variations, any
person or animal is diabetic in proportion as islands of Langerhans
are lacking, and this anatomic fact is so thoroughly established that
it is independent of clinical complexities. Whereas the uncertainty
of diagnosis might formerly be imputed solely to the ignorance of
the pathologist, the latter should now be able to recognize diabetes
positively in any case of fatal severity, without regard for func-
tional differences, from the anatomic deficiency of island tissue
alone, and to form also some idea of the degree of true severity.
When islands are so abundant as to make the diagnosis on this basis
doubtful, the pathologist may say positively that, barring disobedi-
ence, complications, or other uncontrollable accidents, death was due
to inadequate treatment and not to actual severity of the diabetes.

642 CHAPTER vxn

Several trials have been made of the diagnosis of unlabelled pan-
creas specimens from various sources. In brief, when the fixation
has been good and the diabetes severe, the distinction from miscel-
laneous non-diabetic material, on the combined basis of vacuolation
and scarcity or "atrophy" of islands, has succeeded in almost 100
per cent of cases. When either the fixation was poor or the diabetes
mild, mistakes have been so numerous that the results were
largely unreliable.

The confusion concerning pancreatic pathology in the past has
wrongfully cast doubts upon the pancreatic origin of diabetes, not-
withstanding the wide discrepancies between structure and function
freely recognized for other viscera. More accurate correlation of all
the facts, clinical, experimental, and anatomic, justifies the inquiry
with what other organ or disease is the relation between function
and structure so clear and demonstrable as in the case of the pancreas
and diabetes.

C. Relation to Treatment.

For their therapeutic significance, the anatomic changes are again
conveniently divisible into those caused by and causing the diabetes.

1. Hydropic Degeneration. — Clinically, three lessons stand out.
One is the establishment of diabetes as an independent condition with
a pathology of its own. On the one hand, this contributes further to
clear away the pernicious confusion of diabetes with non-diabetic
forms of clinical and experimental glycosuria. On the other hand,
diabetes is raised above the rank of a mere symptom of pancreatic
disease. Its right to recognition as a distinct morbid entity has long
been generally acknowledged because of its importance and its broad
chnical characteristics. It is now seen to have a pathologic course
independent of the inflammatory or other basis on which it arose.
Treatment of diabetes by diet therefore is not mere palliation of a
symptom, but is a genuine means of checking the progress of a
definite pathologic change.

Second, anatomic guidance is given for the direction, ideals,
and limitations of dietotherapy. It emphasizes the need of beginning
at the earhest possible stage, when islands are most abundant and
the power of regeneration perhaps also exists. The fact should be

ETIOLOGY AND PATHOLOGY 643

emphasized that, whatever excuses may be made for lax treatment,
it is responsible for progressive destruction of islands of Langer-
hans. With grossly excessive diet and flagrant symptoms the loss
is rapid; with only hyperglycemia and perhaps traces of acidosis
it is slower; also the susceptibility to functional overstrain differs
widely in different cases; but the ultimate injury manifests itself
clinically, without exceptions other than a few cases so mild that
they tend strongly to recover. Frequently the patient comes
under thorough treatment only after his own carelessness or a physi-
cian's mistakes have caused irreparable downward progress. In the
stage of greatest severity, exemphfied by most of the cases of the pres-
ent series, the remaining island tissue is very scanty, and any ca-
pacity of regeneration seems to be exhausted. The inability to re-
cover assimilative power, and the difficulties in any research aiming
at a cure of such cases, are made clear by this depletion not only of
islands but apparently also of the cells in ducts or elsewhere which are
able to form islands. The purpose of diet is therefore to prevent the
specific degeneration of the islands by relieving functional overstrain.
It obviously cannot check destruction by progressive inflammatory
or other processes. There is also a bare possibility that Weichsel-
baum's "atrophy" may represent a hopelessly progressive disease
of the islands. Experience shows, however, that the signs of pro-
gressive inflaramatory change are usually greatest in the more elderly
patients, whose diabetes is as a rule milder and easier to control,
while in a large proportion of youthful patients the progressive loss
of islands is due chiefly to hydropic degeneration. As mentioned,
the animal experiments demonstrate the possibility of preserving the
islands and the tolerance by restriction of all classes of food in the
absence of any progressive tendency. Though the clinical results are
marred by faults of patients and by mistakes in the apphcation of
the treatment, they prove that in at least a large proportion of cases
an existing downward progress can be checked and a stationary or
improved assimilation maintained through months or years. To date,
as far as the principle of total dietary regulation has been faithfully
carried out, only one case has yet been observed of apparent
"spontaneous downward progress" in absence of the metaboHc injury
of improper diet or infectious complications. Therefore, whatever

644 CHAPTER VIII

part may be assigned to the causes back of the diabetes, it must be
concluded that degeneration of islands due to errors in dietetic man-
agement has been a leading factor in the supposedly "spontaneous"
aggravation of the condition.

Third, a verdict on the treatment can in large measure be given
from the autopsy. Weichselbaum and Stangl's cases were doubtless
treated by the former orthodox method, and the hydropic degenera-
tion found in a majority of them is positive proof of rapid destruction
of islands due directly to the diet. Allowance must be made for dis-
obedience, intercurrent infections, and other uncontrollable accidents.
Otherwise, the finding of hydropic changes condemns the treatment.
Vacuolated islands are not present with thorough dietary control.
It seems possible also to form a correct anatomic judgment of the
true severity of the diabetes. With close distinctions between prep-
ositions, it may be said that many patients die with or from, but
very few of diabetes. They die with diabetes if they are carried off
by some extraneous cause. They may die from diabetes indirectly, if
death results, for example, from infection for which diabetes is re-
sponsible through lowering resistance; or more directly, if the diabetes
reaches such intensity that fasting fails to avert coma, even though
the pancreas contains nmnerous islands and, if coma is barely escaped,
a correspondingly high food tolerance is subsequently attainable.
These deaths, in other words, are due essentially to avoidable acci-
dents of infection, fat intoxication, etc. But with the fundamental
definition as deficiency of the internal secretion of the pancreas, a
patient can be said to die strictly of diabetes only when this secre-
tion is absolutely too scanty to support life. These are the patients
who cannot be free from active symptoms except at the price of
extreme emaciation, who cannot gain appreciably in assimilative
power, and who sometimes die finally of inanition in spite of unbroken ,
fidelity on their own part and the best skiU of the physician. Irre-
spective of any assmned functional alterations, the few autopsies
upon such patients to date have invariably shown an organic dearth
of island tissue fully siifiicient to explain the hopeless clinical severity.
The failure of treatment has thus been due to inability to replace the.
islands, which have been lost probably to some extent in an inflam-
matory process, but in most cases largely through previous errors in
dietetic management.

ETIOLOGY AND PATHOLOGY 645

Certain points should also be mentioned in which the autopsy is not
decisive concerning treatment. First, absence of discoverable hy-
dropic change does not prove that the diet was suitable, since, as
mentioned above, a certain intensity of overstimulation is necessary
before this change is apt to be discoverable. Second, even extreme
dearth of islands along with absence of vacuolation does not neces-
sarily relieve the physician of responsibility for the death. It largely
absolves firom any accusation of acute death due to avoidable acci-
dents. But it has been a common mistake to feed patients slightly
beyond their true tolerance, permitting hyperglycemia and sUght
acidosis for the sake of temporary subjective comfort, and checking
more serious symptoms by occasional fasting or reduced diet. In
this way downward progress is merely delayed; the breakdown of
islands by functional overstrain occurs more slowly but just as in-
evitably. Finally, thfe most rigid treatment may be unavailing be- ,
cause the pancreatic capacity has fallen actually too low to support
life; but the cause may have been not a chronic progressive tendency
of the disease but a chronic inefl&ciency of treatment.

2. Changes Causing Diabetes. — The inflammatory origin of diabetes
carries distinct therapeutic significance. Islands once destroyed can-
not be replaced by any means now known. AU that can be hoped is
to spare the function of the remainder as effectually as possible by
diet, and thus also to provide the most favorable conditions for spon-
taneous regeneration. Acute inflammation as a cause of diabetes
offers tiree suggestions: first, the importance of sparing the weakened
function from the outset; second, the desirability of finer methods
for the diagnosis of pancreatitis, along with surgical or other pro-
cedures to mitigate the consequences; third, the chance that in at
least some cases the organic lesion may not progress further and the
subsequent welfare may be purely a question of whether the remain-
ing islands are spared or destroyed by diet. As far as diet was prop-
erly conducted, the present series supports this expectation, by
showin_g the apparent absence of inherent progressive tendency in a
considerable proportion of cases. With early eflacient dietary care, it
is to be hoped that the small number of more or less complete cures,
such as cases Nos. 40 and 76 in this series, case No. 203 of Joslin,'"

'« Joslia, E. P., Treatment of Diabetes MeUitus, 1917, p. 52.

646 CHAPTER VIII

and the extreme example of Jonas and Pepper,^' may somewhat in-
crease. Chronic inflammation makes a direct appeal for some thera-
peutic intervention to stop it. With improved dietetic control, more
attention is undoubtedly going to be paid to the diagnosis of chronic
pancreatitis and to attempts to prevent the injury which it pro-
duces as respects both diabetes and the general health. By reason
of the relative safety with which operations can now be performed
upon properly prepared diabetics, explorations for the cause of pan-
creatitis, the removal of otherwise quiescent gall stones and the
drainage of infected bile will probably become more common, especi-
ally perhaps in cases at or beyond middle Hfe. The conception of
diabetes as due chiefly to pancreatic inflammation creates a more
hopeful general view-point than before. The pathologic study thus
offers the first well grounded hope that, as constantly better control
of infectious disease is achieved, the race may some time be free of
diabetes.

Conclusions.

1. The status of the islands of Langerhans as an internal secretory
organ and as the seat of the specific diabetic disturbance is now as
firmly estabUshed as any fact in physiology or pathology. In addi-
tion to the older extirpation and ligation experiments, which were
not conclusive, the new evidence consists in the production of diabetes
with large masses (up to one-third of the pancreas) of normal appear-
ing acinar tissue present when only islands are deficient, and es-
pecially in the occurrence of visible exhaustion and degeneration of the
island cells in demonstrable parallelism with variations in diet and
the course of the diabetes.

2. CUnical diabetes apparently arises regularly on a basis of pan-
creatitis, either acute or chronic; and with accurate correlation of
chnical and anatomic examinations, a geneirally logical association of-
function and structure is perceptible.

3. The explanation of the permanent lowering of assimilation re-
sulting from excess of any kind of food in diabetes is the specific de-
generation of the islands of Langerhans thus produced. Regulation
of the total diet is not merely the treatment of a symptom, but is the
essential means of preventing the principal cause of downward progress.

"Jonas, L., and Pepper, O. H. P., J. Am. Med. Assn., 1917, kviii, 1896-1897.

TABLE III.

Diet.

Body
weight.

Fluid.

Urine.

Gm. „,
Cal. "'

i

.2

S

"id

Foodstuffs.

Remarks.

1

3
O

CC.

d

Reaction.*

Dextrose.*

FeCla

Nitroprasside.

1

Date.

2

1

u

a

Cm

i

1

im.

Eacon.

i

gm.

m
gm.

gm.

6

.a
O

gm.

Vegetables.

t

1

2

3

4

1

2

3

4

Gm.

gm.

ft
•c
o

gm.

gm.

o

P

6

d

o
in

19i7

gm.

s«.

gm.

gm.

gm.

gm.

gm.

gm.

ig.

cc.

gm.

gm.

Sept. 23
" 29

Fa St- day.

22.5

ii

150

ti

600

3

4 bran muffins.

a it it

43.5
42.0

1050
1050

585
785

1025
1015

Ac.

it

Ac.

ii

Ac.

Ac.

a

H.

Slight.

H.

Faint.

H.
Faint.

Mod.

Neg.

12.87

5.03
6.02

Mod.

V.H.
H.

1.05

0.71

" 30

10
41

5.3

21

0.3

2

64

358

ii

ii

ii ii it

ii

1450

1770

1008

it

ii

it

31. Ac.

Neg.

Neg.

Neg.

it

0

5.57

SI.

li

0.63

Oct. 1

20

82

7.8

31

1.3

12

125

629

ii

ii

it a it

42.3

1850

1305

ii

it

li

ii

Ac.

ii

it

a -

it

0

4.77

Faint.

Mod.-t-

0.20

" 2

30

123

10.5

43

2.6

24

190

796

ii

ii

ii ii a

42.0

1650

2245

1006

a

u

ti

ii

it

ii

it

it

0

5.61

It

H.

0.27

" 3

40

164

14.2
58

3.2

29

251

990

ii

iC

6 "

ti

2056

2405

1005

N.

l(

a

SI. Ac.

ii

ii

a

it

0

4.09

it

ii

0.24

" 4

50

205

15.4
63

3.3

30

312

1094

ii

ii

a ii it

ti

1950

2625

li

a

li

SI. Ac.

ii

li

li

a

"

0

3.25

it

it

0.21

" 5

60

246

17.0
69

3.4
31

346

1232

ii

ii

ii ii it

41.3

2050

2330

it

it

N.

it

N.

ii

ii

a

ii

0

4.66

ti

Mod.+

0.14

" 6

70

287

19.3

79

3.8

35

401

1339

ii

ii

a it ii

41.0

1850

2853

it

it

it

it

S!. Ac.

ii

It

V. faint.

it

0

5.14

a

Mod.

0.11

" 7

80

328

20.5

84

4.2
39

451

1459

ii

ii

a it a

41.2

ii

3180

li

a

a

Ac.

N.

it

a

Neg.

V. faint.

0

6.30

it

ii

0.13

" 8

90

369

24.0

98

4.0

37

504

1433

ii

ii

a ii it

40.0

it

2255

ii

ti

81. Ac.

ii

ii

it

Faint.

Faint.

it

5.41

Neg.

a

a

" 9

Fast-day.

300

45

ii

ii

a it a

40.1

1250

1230

li

Ac.

Ac.

ii

Ac.

ti

Neg.

Neg.

Neg.

0

5.48

Faint.

a

0.21

" 10

30.0

123

3.1

28

. 151

Chicken.
63

72

600

ii

ti

ii

2 cups agar jelly.
8 bran muffins.

39.9

1050

1845

1010

a

SI. Ac.

ii

ii

it

it

it

ti

0

9.41

Neg.

it

0.63

" 11

30.0

123

1.8

16

139

Egg white.
41

32

72

1000

ii

ii

ii

(( a if

li

1450

1365

1008

ti

ii

ii

li

it

ti

it

ii

0

9.62

ii

Sl.-i-

0.56

" 12

30.0

123

1.8
16

ii

{(

ii

ii

a

ti

ti

it

a it It

39.5

1250

1233

1010

it

Ac,

ii

a

li

it

it

ii

0

7.14

Faint.

ii

0.39

" 13

30.0

123

1.8
16

ii

((

u

ii

a

ii

it

a

a it ii

ii

1450

1365

1005

it

ti

ti

ii

it

ii

it

ii

0

9.77

a

ti

0.16

" 14

30.0
123

1.8
16

a

a

a

ii

ii

ii

ii

it

a a it

39.1

1850

2615

1008

it

a

ii

it

ii

it

it

it

0

,

Neg.

V. Faint.

" 15

30.0

123

1.8
16

l(

u

ii

ii

a

ii

ii

a

it ti ii

38.9

1450

1725

li

a

li

ii

it

ii

it

it

it

0

_

it

SI.

" 16

Fast-day.

ii

ii

it

a

a a it

38.7

1650

1230

1013

ii

ii

ii

li

it

it

it

ii

0

—

it

S1.+

—

" 17
" 18

10

41
10
41

30.0

123

40

164

2.6

24
4.5
41

188
246

82

ii

40
82

72

ii

292

ii

ii
ii

' ii
ii

ii
ii

ii
ti

2 cups agar jelly.
8 bran muffins.

it t< ti

39.3
38.4

ii
ii

1542
1370

1012

u

it
a

a
it

ii

if

it
ii

it
ii

it
ti

a
ii

it
ii

0
0

—

It
a

Faint.

—

" 19

10

41

50.0

205

4.5

45

291

a

ii

144

(i

ii

. it

ii

t'

ii ii it

39.1

1250

1720

1014

it

it

it

ii

it

ti

it

ii

0

.

a

Neg.

—

" 20

10
41

60. C

246

7.2
66

353

it

144

72

a

ii

a

it

a

a it a

ii

1450

1725

1010

it

ii

li

it

it

ti

ti

ii

0

li

ii

_

. " 21

10

41

60.0
246

20. C

186

473

Beef.
97 62

117

13

ii

ii

it

it

it

it

a a it

39.3

li

1842

a

a

a

it

it

is

it

ii

li

0

ti

ti

—

" 22
" 23

10

41
Fas

60. C
246

-day.

30. (

279

)

566

200

49

72

7

ii

ii
it

it

it

it

it

ii
ii

it
a

a a ti
it a It

39.4
39.0

ii

1550

1770
1430

1008
1009

li
ii

ti
it

ii

ii

"

li
it

a
li

it
a

ii ■
ii

0
0

—

it

11

ti

—

" 24

10

41

60. C

246

40. (

372

)

659

200

49

77

19

it

it

it

a

it

it

2 cups agar jelly
8 bran muffins.

39.3

1450

1689

ii

li

ti

it

it

it

ti

ii

it

0

n

a

—

" 25

10

41

60. C
246

) 60. (

558

3

845

200

82

42

ii

u

u

ii

a

a

it it a

ii

ii

1700

it

it

ii

ii

a

ii

a

it

"

0

11

<4

—

" 26

10

41

60. (

246

) 80. (

744

3
1031

200

66

50

26

Dh

:iitiz

@d bv Mic

rose

:ft®

;

* The four columns represent the four periods into which each day's urine is divided.

TABLE III.

Urine.

Blood.

trose.*

FeCls

Nitroprusside.

i

Acetone bodies as acetone.

3

<

Remarks.

Plasma.

1

Total fatty acid.

Cholesterol.

Lecithin.

3

4

Gm.

t-i

1^

&

o

4.11

3.52

i

lis

+1

sis

<

■32.

u ft

6

i

s

1

4,

1

ft
►3

o

1

'6
J

1

J

CM

a
o
U

■g

o
'o

;3

&

o

o

o

&

o
U

Remarks and clinical notes.

H.
"aint.

Mod.

Neg.

12.87

gm.
5.03
6.02

H.

Mod.

V.H.
H.

gm.
1.05

0.71

gm.

gm.

1.05

2.48

gm.
3.12
1.04

cc.

205
215

Neg.

10:30 a.m.
11:30 "

per cent

0.227
0.106

vol.
per cent

64.3
58.6

mg.
12

12.5

mg.

26.0
43.7

mg.

38.0
56.2

++
++

+

Neg.

per cent

85
103

per cent
44.6
46,2

per cent

1.63
0.95

per cent

1.75
1.02

Per cent
1.32
0.93

per cent
0.60
0.55

per cent

0.65
0.59

per cent

0.42
0.51

per cent

0.25
0.21

per cent

0.19
0.14

per cent
0.31
0.26

Patient admitted.

Neg.

iC -

a

ii

ii
li

0
0
0

S.S7
4.77
5.61

SI.

Faint.
ii

li

Mod.+
H.

0.63
0.20
0.27

1.49
1.71
1.19

1.96
1.34
0.75

3.45
3.05
1.94

199
200
195

ii
CI
ii

Carbohydrate test begun.

li

li

a

0
0

4.09
3.25

a
a

li
ii

0.24
0.21

0.30
0.42

0.35
1.08

0.85
1.50

130
117

li

ii

iC

ii

0

4.66

a

Mod.+

0.14

0.44

0.51

0.95

65

ii

faint.

li

0

5.14

ii

Mod.

0.11

0.31

0.63

0.94

35

ii

Neg.

V. faint.

0

6.30

a

11

0.13

0.13

0.29

0.42

75

it

"aint.

Neg.

ii
ii
ii

Neg.

a

0

0
0
0

5.41
5.48

9.41
9.62
7.14

Neg.
Faint.

Neg.

a

Faint.

li
(I

li

S1.+

ii

it

0.21

0.63
0.56
0.39

0.18
0.27

0.27
0.37

0.45
0.64

51
160

220
231
216

it

ii

li
it

9:30 a.m.

0.133

63.2

Tr.

36.2

36.2

0

0

99

45.3

0.57

0.63

0.52

0.42

0.45

0.39

0.19

0.13

0.23

End of carbohydrate test.
Beginning of low calory diet to clear up
hyperglycemia and ketonuria.

it

ii

0

9.77

it

it

0.16

—

—

—

211

it

a

a

0

—

Neg.

V. Faint.

—

—

—

—

—

"

"

li

ii

0
0

—

it

SI.
S1.+

—

—

—

—

—

li

5:00 p.m.
12:00 n.

0.123

li

64.4
71.0

Neg.

11

13.2
11.3

13.2
11.3

0
0

0
0

98

li

47.7
51.0

0.55
0.57

0.61
0.60

0.50
0.55

0.38
0.40

0.41
0.43

0.37
0.39

0.23
0.21

0.17
0.16

0.29
0.24

Weekly fast-day.

ii

a

0

—

U

Faint.

—

—

—

—

—

—

10:00 a.m.

0.083

69.1

li

7.0

7.0

0

0

96

52.0

0.61

0.65

0.59

0.32

0.36

0.30

It

0.19

0.23

a

ii

0

—

it

11

—

—

—

—

—

—

it

a

0

—

u

Neg.

—

—

—

—

—

—

a

a

0

—

n

it

—

—

—

—

—

9:30 a.m.

0.076

68.1

—

—

—

0

0

101

44.5

0.51

0.56

0.49

0.26

0.30

0.21

0.30

0.28

0.38

ii

a

0

—

a

it

—

—

—

-

—

10:15 "

0.123

62.4

—

—

—

0

0

98

37.2

0.53

0.54

0.51

0.28

it

0.26

0.29

0.24

0.32

i(
it

ii ■

a

0
0

—

tt

li

—

—

— "

—

10:00 "

0.104

62.3

—

0

0

96

39.8

0.49

ii

0.45

0.31

0.36

0.29

0.21

0.18

0.27

Weekly fast-day.

it

a

0
0

—

((

it

-

—

-

-

-

-

5:15 p.m.

0.114

Dig

67.2

'tize

dlb)

' Mk

:ros

0

0

98

46.0

0.52

0.56

0.49

0.25

0.27

0.21

0.32

0.27

0.38

CUHBOHTDRATE

Cjojokos

96«

to;

«H.

46

SO

«0

Kt

M

4.]

SOAP

52.6

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General data.

Family history.

Past history.

Sex.

Nationality or
race.

Age.

Occupation.

Diabetes..

Obesity.

Tuberculosis.

Other disorders.

Infections and accidents-

Nervous system.

Activity.

Habits.

Figure.

Digestion.

.a
e

Childhood.

Adult.

Wasser-
mann test

Alcohol.

Tobacco.

Appetite and
diet.

Boi

1

F.

American.

yrs.
28

None.

Uncle (1).

Father, tendency
to melancholia.
Sister, nephritis.

Measles, diarrhea.

Naturally nervous ;
unhappy love
affair.

Overs treiiuous
socially.

Fond of eat-
ing; excess
in sweets.

Thin.

Good.

Moder
stipa

2

Italian.

17

Sewing ma-
chine oper-
ator.

Father; broth-
er (moder-
ate).

u

Phlegmatic.

Swpat-shop.

i

Slight.

Moderate.

Slightly
obese.

Regula

J

M.
F.

American.

26

None.

Maternal
grandfather;
father; un-
cle.

Maternal aunt
died of melan-
cholia. Brother
nervous.

" mumps; chick-
en-pox; typhoid; ton-
sillitis.

"Colitis;" grippe; inter-
costal rheumatism; ap-
pendicitis; appendec-
tomy; oophorectomy;
phlebitis.

Sensitive.

Some social
strain.

1

•

Much candy.

Normal.

u

i

4

12

Sister; pater-
nal grand-
father; un-
cle.

Maternal grand-
mother, cancer.
Neurotic on
father's side.

Abscess on neck; bron-
chitis; rheumatism;
measles; chicken-pox;
tonsillitis.

Precocious; neu-
rotic.

Normal.

-

Sweets re-
stricted.

Plump.

a

6

34

Customs in-
spector.

-

Measles; tonsillitis.

Gonorrhea; acute pan-
creatitis (?).

Neurotic.

\
i

Occasional ex-
cess.

Moderate.

Irregular.

Normal.

Poor.

Consti

0

Italian.

48

Housewife.

(Husband now

diabetic. Patie

nt very ignoran

t.)

Unknown.

Phlegmatic.

Tenement life.

Slight.

No excess.

Slightly
obese.

Good.

Regula

/

American
(Swedish) .

36

Saleswoman.

Scarlet fever.

Miscarriage.

Nervousness per-
haps due only
to diabetes.

Unhappy mar-
ried life.

Excess (?).

Light eater;
coffee to
excess.

Obese.

i(

a

8

M.

a

i(

F.
M.

American.

29

Printer.

Mother, simple
goiter.

Measles; chicken-pox;
mumps.

Slight pleurisy.

—

Normal.

Normal.

Little.

Little.

No excess.

Thin.

a

Slightl)
stipa

y

Jew.

24

Tailor.

-•#

(Memory uncertain.)
Rheumatism.

Gonorrhea; bronchitis;
frequent colds.

Neurotic.

! il

1
i

Moderate.

Ordinary.

Normal.

Constif

10

American
(Irish).

17

Plumber.

Measles; whooping-
cough.

Normal.

Healthful.

i

Large; much
sweets.

u

((

Regula

11

Austrian.

55

Housewife.

Obese family.

Measles.

4 miscarriages.

i(

Ordinary.

Slight.

Excess de- .
nied.

Very obese.

a

a

12

Jew.

49

Tailor.

Moderate.

Partial tonsillectomy.

ti

I

1

a

Moderate.

No excess.

Obese.

iC

il
1

Digitized by Microsoft©

TABLE 1— General Summary.

Past history.

Diabetic history.

Activity.

Habits.

Figure.

Digestion.

Bowels.

Onset.

Glycosuria discovered.

Weight.

Polypha-
gia.

Polydipsia

and

polyuria.

Pruritus.

Skin infections.

Albuminuria.

Menstruation or
sexual function.

Pains.

Alopecia.

Ac

system.

Alcohol.

Tobacco.

Appetite and
diet.

Acute or
gradual.

Date o-f first
symptoms.

Time.

Cause of examina-
tion.

Highest.

At
onset.

At
admis-
sion.

Degree.

^nervous;
)y love

Overstrenuous
socially.

Fond of eat-
ing ; excess
in sweets.

Thin.

Good.

Moderate con-
stipation.

x\cute.

Jan., 1913

July 6, 1913

Polydipsia ; poly-
phagia; pru-
ritus.

kg.
56.8

kg.

kg.

40.1
42.6

+

. +

Marked.

-

Stopped May,
1913.

Marked.

Heavy.

+

ic.

Sweat-shop.

Slight.

Moderate.

Slightly
obese.

il

Regular.

Gradual.

Dec, 1912

Mar. 14,
1913

Weakness; loss
of weight;
polyphagia;
polydipsia.

5.45

40.9

+

+

Stopped Feb.,
1913.

Headaches.

Moderate.

Some social
strain.

Much candy.

Normal.

ii

-■^cute.

Jan., 1913

May, 1913

Weakness; loss
of weight.

54.5

49.5

46.5

+

+

Normal.

Marked.

a

is; neu-

Normal.

Sweets re-
stricted.

Plump.

a

ii

Summer,
1907

Immediate.

Polyphagia;
polyuria.

31.8

23.8

+

+

Two ulcers.

Slight 1st 15
days; slight
terminal.

Neuritic in
legs.

Slight.

Heavy at
times.

+

Occasional ex-
cess.

Moderate.

Irregular.

Normal.

Poor.

Constipated.

a

July, 1913

Sept., 1913

Polydipsia; loss
of weight and
strength.

79.5

72.3

60.4

+

+

Faint 1st 11
days.

Lessened libido.

Back and legs.

Present, but
not con-
nected with
diabetes.

Slight.

ic.

Tenement life.

Slight.

No excess.

Slightly
obese.

Good.

Regular.

Unknown.

July 25,
1914

Hospital rou-
tine.

58.8

Faint 1st 15
days.

Climacteric 1913.

i(

ess per-
ue only
etes.

Unhappy mar-
ried life.

Excess (?).

Light eater;
coffee to
excess.

Obese.

u

Acute.

Dec, 1913

Mar., 1914

Pruritus; loss of
weight.

76.3

52.8
50

+

Vulvar,
marked.

Superficial vul-
var; also

styes.

Faint, transi-
tory.

Normal.

Severe in legs.

Marked.

ii

Normal.

Little.

Little.

No excess.

Thin.

ii

Slightly con-
stipated.
Constipated.

ii

June, 1913

June, 1913

Polydipsia.

68.2

+

+

—

Absent.

Slight.

Heavy.

+

a

a

Moderate.

Ordinary.

Normal.

ii

ii

Oct., 1913

Oct., 1913

Bronchitis.

68.2

53.6

+

+

Headaches.

it

Healthful.

Large; much
sweets.

a

ii

Regular.

ii

Jan., 1914

June, 1914

Polydipsia; loss
of weight.

60.5

41.6

+

+

Cervical swell-
ing of un-
known na-
ture.

Moderate 1st 3
days.

ii

+

Ordinary.

Slight.

Excess de-
nied.

Very obese.

ii

a

Gradual.

1904

1907

Bitter taste;
constipation.

91.3

74.2

Heavy.

Stopped.

Head, thorax,
and abdo-
men.

Beginning.

a

+

it

ii

Moderate.

No excess.

Obese.

il

ii

Acute.

1911

Immediate. Weakness; poly- 91
dipsia.

DiQitized by Microsoft®

86

Transi-
tory.

Transi-
tory.

Slight.

Lichen planus
of arms; ul-
cers of feet.

Faint

Normal .

Neuritic in
back and
legs.

Present, not
due to dia-
betes.

Slight.

Physical examination.

Menstruation or
sexual function.

Pains .

Alopecia.

Acidosis.

Complexion.

Nutrition.

Thyroid.

Teeth.

Tonsils.

Heart.

Lungs.

Liver.

Lymph glands.

Knee jerks.

Blood
pressure.

ria.

Degree.

it

a "
+

Hyperp-
nea.

Digestive
symptoms.

it

2 o

Remarks.

Stopped May,
1913.

Marked.

Heavy.

+

-

Pale.

Emaciated.

Normal.

Good.

Normal.

Normal.

Normal.

Normal.

Normal.

Normal.

103

80

Lower pole of right kidney pal-
pable; incipient coma.

Stopped Feb.,
1913.

Headaches.

Moderate.

Good.

Medium.

a

ti

Slightly hyper-
trophied.

it

a

ti

it

ti

Strong peasant type.

Normal.

Marked.

it

+

a

Good.

It

it

Normal.

a

ti

it

120

Temporary weakness of vision.

t IS
slight

.

Neuritic in
legs.

Slight.

Heavy at
times.

+

Vomiting.

Sallow.

Emaciated.

it

Poorly devel-
oped.

Slightly hyper-
trophied.

ti

ti

it

Slight cervical en-
largeiaent.

Diminished.

ISO

. lis

lis

70

Chronic nephritis; nearly total
blindness from retinitis.

t 11

Lessened libido.

Back and legs.

Present, but
not con-
nected with
diabetes.

Slight.

a

Fair.

it

Poorly devel-
oped.

Hypertrophied;
no pus foci.

ti

Normal at first;
subsequent hy-
pertrophy and
atrophy.

Slight general
adenopathy.

Normal.

Cirrhosis of liver.

t 15

Climacteric 1913.

a

-

Cyanotic.

Good.

Caries; pyor-
rhea.

Hypertrophied;
congested;
no pus foci.

Hypertrophied.

Lobar pneu-
monia.

Edge felt at costal
margin.

Normal.

Sluggish.

Admitted for pneumonia.

ransi-

Normal.

Severe in legs.

Marked.

a

Fair.

Fair.

ti

Fair; consider-
abte tartar.

Normal.

Normal.

Normal.

Normal.

Slight posterior
cervical enlarge-
ment.

Normal.

60

75

95

Uterus retroflexed and retro-
verted.

Absent.

Slight.

Heavy.

+

+

Nausea.

Pale.

Emaciated.

It

Good.

it

a

tt

a

Slight epitrochlear
enlargement.

Pulmonary tuberculosis later de-
veloped.

Headaches.

a

Colic; nau-
sea; vom-
iting.

Flushed.

Poor.

it

Caries; pyor-
rhea.

a

Bronchial rales
at apices.

tt

Normal.

Absent.

80

Hemoptysis once; persistent
bronchitis, clearing up on
treatment; tuberculosis never
demonstrated.

1st 3

i(

+

+

Nausea.

Pale.

Emaciated.

it

Caries.

it

ti

Normal.

ti

a

ti

85

Dangerous weakness and acidosis
at admission.

Stopped.

Head, thorax,
and abdo-
men.

Beginning.

a

+

+

vomiting.

Cyanotic.

Obese.

it

All missing.

it

Mitral regurgi-
tation.

Congested from
heart failure.

Edge felt 2 cm.
below umbilicus.

it

Orthopnea, hemoptysis, and all
signs of heart failure.

Normal.

Neuritic in
back and
legs.

Present, not
due to dia-
betes.

Slight.

Good.

ic

" Caries; pyor- Hypertrophied. Normal.
rhea.

Digitized by Microsoft®

Slight emphy-
sema.

Normal.

a

Normal.

1.S0

Chronic bronchitis; hemoptysis
three times; varicose veins and
eczema on legs

General data.

Family history.

Past history.

1

Sex.
F.

Nationality or
race.

Age.

Occupation.

Diabetes.

Obesity.

Tuberculosis.

Other disorders.

Infections and accidents.

Nervous system.

Activity.

Habits.

Figure.

Digestion.

u

S

Childhood.

Adult.

Wasser-
mann test.

Alcohol.

Tobacco.

Appetite and
diet.

Bowels.

13

American.

. yrs.
11

Schoolgirl.

Paternal grand-
father, cancer.

Whooping-cough; mea-
sles; mumps; adenoids
removed.

-

Normal.

Quiet life.

Normal.

Rather
thin.

Good.

Regular.

14

M.

a

F.

M.

Jew.

51

Optician.

Scarlet fever.

Occasional sore throats;
gonorrhea twice; dry
pleurisy.

a

Ordinary.

Moderate.

Moderate.

Rather
small.

Thin.

Slight dys-
pepsia.

Constipated.

15

Scotch.

42

Boolikeeper.

(Nothing hereditary known to t

(vife.)

(Healthy life

. History imperfect. )

11

it

Little.

it

Normal.

Normal.

Good.

Regular.

IB"

Jew.

47

Housewife.

Mother;
brother.

.

Father, cancer.

Measles; mumps.

Syphilis.

+ + + +

it

it

Moderate.

ti

Slightly
obese.

li

it

17

it

69

it

(Negative as

ar as known.)

Daughter, demen-
tia precox.

it

Pneumonia with empy-
ema; 3 operations;
laparotomy for tumor.

it

it

Little. -

a

SUghtly
obese.

Slight indi-
gestion.

Constipated.

.18

American.

16

Errand boy.

Father, cirrhosis
of liver.

Chicken-pox; tonsillitis.

it

it

Little.

it

Normal or
slightly
thin.

Good.

Regular.

19

F.

Jew.

39

Housewife. . .

Measles; whooping-
cough; typhus.

Peritonsillar abscess;
puerperal sepsis; 1
miscarriage.

it

it

Little.

Small.

SUghtly
obese.

a

it

20

American.

38

a

Brother.

Scarlet fever; measles;
chicken-pox; whoop-
ing-cough; diphtheria.
Fall at age of 2.

Recent sore throat.

Nervousness; mi-
graine.

a

No excess.

Normal.

a

ti

21

ii

M.

a
it

Scotch.

46

a

Measles; mumps; whoop-
ing-cough.

Scarlet fever; ventral
hernia operation; sore
throats.

Slightly nervous.

it

ti it

Very obese.

it

it

22

Jew.

52

Cigar manu-
facturer.

Mother, nephritis.
Sister, cancer.

Gonorrhea twice.

Very nervous.

Intense business
strain.

Considerable.

Excess.

Luxurious
living.

Thin.

a

Constipated.

23

American.

44

Insurance
agent.

Mother.

Measles; chicken-pox;
mumps.

Gonorrhea; "bloody dys-
entery."

Normal.

Some business
worry.

Moderate.

Moderate.

Normal.

Slightly
obese.

u

Regular, v

24

it

44

Manufacturer.

Father.

Paternal aunt,
cancer.

Measles; mumps; otitis.

Digitizec

Gonorrhea; acute articu-
lar rheumatism; sore
throats; acute pancre-

b^itMmrosoft®

It

Ordinary.

Little.

Much.

it

Thin.

Poor.

Constipated.

TABLE I-(

Continued.

listory.

1

Diabetic history.

kd

Habits.

Figure.

Digestion.

Bowels.

Onset.

Glycosuria discovered.

Weight.

Polvpha-
gia.

Polydipsia

and
polyuria.

Pruritus.

Skin infections.

Albuminuria.

Menstruation or
sexual function.

Pains.

Alopecia.

iosis.

y-

Alcohol.

Tobacco.

Appetite and
diet.

Acute or
gradual.

Date of first
symptoms.

Time.

Cause of examina-
tion.

Highest.

kg.
26.8

At
onset.

At
admis-
sion.

Degree.

s s
+

Hyperp-
nea.

Digestiv(
symptom;

Normal.

Rather
thin.

Good.

Regular.

Acute.

Apr., 1914

Apr. 21,
1914

Slight languor.

kg.

26

kg.
21.2

-

-

Moderate 1st 5
days.

Back and
bladder.

Marked.

Heavy.

+

-

Moderate.

Moderate.

Rather
small.

Thin.

Slight dys-
pepsia.

Constipated.

Gradual.

1907

Summer,
1907

Backache.

63.6

51

50.8

Lessened libido.

Neuritic in
back and
legs.

Beginning.

Shght.

Little.

Normal.

Normal.

Good.

Regular.

I'

1912

1912

Slight loss of
weight and
strength.

Present, not
known to be
due to dia-
betes.

Heavy.

Moderate.

u

Slightly
obese.

u

a

It

1909

1909

Weakness; loss
of weight.

81.7

72.6

65

+

Vulvar,
moder-
ate.

Moderate to
slight.

Regular till cli-
macteric 1914.

Head and
legs.

Beginning.

Slight.

Little.

((

Slightly
obese.

Slight indi-
gestion.

Constipated.

About 1907

Oct., 1914

Gangrene.

82

49.1

53.6

+ +

Incipient gan-
grene of foot.

Slight.

Foot.

Probably only
senile.

Insignificant.

Little.

((

Normal or
slightly
thin.

Good.

Regular.

Acute.

Oct., 1914

Nov., 1914

Lassitude; poly-
phagia; poly-
dipsia.

60.5

50.6

+

+

Slight.

Slight 1st 5 days.

-

Little.

Small.

Slightly
obese.

((

ii

Gradual.

May, 1913

Oct., 1914

Pruritus; poly-
phagia; poly-
dipsia; loss of
weight.

66.3

49.1

47.2

+

+

Vulvar,
marked.

Faint 1st 23
days.

Stopped.

Head and
back.

Slight.

Insignificant.

Nausea;
colic.

No excess.

Normal.

(I

it

tt

Oct., 1913

1913

Hospital rou-
tine.

77

72.8

53

Faint 1st 22
days.

Normal.

Head.

Slight.

It It

Very obese.

Ci

It

Acute.

Summer,
1914

1914

Polyphagia;
polydipsia;
loss of weight.

Ocular examina-
tion.

121

105

108

+

+

Faint.

till
menopause.

Slight.

usiness

Considerable.

Excess.

Luxurious
living.

Thin.

iC

Constipated.

ti

1912

Nov., 1912

50

+

+

Moderate to
negative.

Impotence for
2-3 yrs.

Cramps in
legs.

Present, not
due to dia-
betes.

Moderate.

t

usiness

Moderate.

Moderate.

Normal.

Slightly
obese.

it

Regular.

Gradual.

1905

1906

Insurance.

88.5

75

70.5

It

Little.

Much.

u

Thin.

Poor.

Constipated.

Acute.

1907

1907

Ocular examina- 75 63.5
tion.

Digitized by /V

44.2 + +

'icrqsoft^

Stopped.

tt

Physical examination.

Menstruation or
sexual function.

Pains.

Alopecia.

Acidosis.

Complexion.

Nutrition.

Thyroid,

Teeth.

Tonsils.

Heart.

Lungs.

Liver.

Lymph glands.

Knee jerks.

Blood
pressure.

ria.

Degree.

ft 8
e s

+

Hyperp-
nea.

Digestive
symptoms.

'n
75

70

Remarks,

1st 5

Back and
bladder.

Marked.

Heavy.

+

-

Flushed.

Emaciated.

Normal.

Good.

Hypertrophied;
no pus foci.

Normal.

Normal.

Normal.

Normal.

Diminished.

lOS
100

Attacks of urinary calculi.

Lessened libido.

Neuritic in
back and
legs.

Beginning.

Slight.

Sallow.

Poor.

It

Many missing;
caries; pyor-
rhea.

Normal.

it

Slight emphy-
sema.

it

Slight general
adenopathy.

Normal.

Slight hemoptysis at time of
pleurisy.

Present, not
known to be
due to dia-
betes.

Heavy.

Cyanotic.

Moderately
emaci-
ated.

it

Good.

it

ti

Normal.

a

Normal.

Absent.

Received in coma.

to

Regular till cli-
macteric 1914.

Head and
legs.

Beginning.

Slight.

Pasty.

Good.

It

Several miss-
ing.

it

Hypertrophied;
mitral regur-
gitation.

ii

Edge felt at costal
margin.

ti

Normal.

225

110

Latent syphilis; chronic nephri-
tis; mitral insufficiency; ar-
teriosclerosis; cystitis.

Foot.

Probably only
senile.

Insignificant.

Poor.

Emaciated.

. It

Many missing;
caries; pyor-
rhea.

it

Hypertrophied.

Slight bronchi-
tis; lower
right lobe
obliterated.

Normal.

Inguinal enlarge-
ment.

11

215

150
60

Senility; bad hygiene; incipient
gangrene of right foot.

days.

-

Fair,

Rather
poor.

it

Good.

Hypertrophied;
no pus foci.

Normal.

Normal.

it

Normal.

Exaggerated.

135

Transitory dimness of vision.

23

Stopped.

Head and
back.

Slight.

Insignificant.

Nausea ;
colic.

Pale.

Poor.

it

Caries; pyor-
rhea.

Normal.

it

■

Emphysema.

it

a

Normal.

90
140

60

Slight edema and nephritic ap-
pearance, but no nephritis.

22

Normal.

Head.

Slight.

Fair.

Fair.

a

Caries; pyor-
rhea.

it

Mitral regurgi-
tation.

Normal.

ti

Axillary enlarge-
ment.

it

110

Marked xanthoma. ,

till
menopause.

Slight.

Good.

Very obese.

Slightly ■
enlarged.

Many missing;
caries; pyor-
rhea.

Hypertrophied;
no pus foci.

Slightly hyper-
trophied.

Emphysema.

It

Normal.

it

175

120

Bilateral arcus senilis; slight al-
buminuria without casts.

to

Impotence for
2-3 yrs.

Cramps in
legs.

Present, not
due to dia-
betes.

Moderate.

Sallow.

Emaciated,

Normal.

Several miss-
ing; caries;
pyorrhea.

Slightly hyper-
trophied.

Hypertrophied.

Normal.

Edge felt 2 cm.
below costal
margin.

General aden-
opathy.

it

135

110

Chronic nephritis; arteriosclero-
sis; hysteric attacks.

u

■"

Good.

Good.

Slight caries.

Hypertrophied;
no pus foci.

Normal.

it

Edge felt 3 cm.
below costal
margin.

Slight epitrochlear
and inguinal en-
largement.

it

Stopped.

it

Sallow,

Emaciated.

Good.

Digitized by

Normal.

IVIicrosonfE)

it

Edge felt at costal
margin.

Normal.

Sluggish.

70

55

Temporarily impaired visioti;
yellow skin; lipemia; erythro-
cytes 4,000,000; extreme weak-
ness.

General data.

Family history.

Past history.

d

Is

Sex.
F.

Nationality or
race.

Age.

Occupation.

Diabetes.

' Obesity.

Tuberculosis.

Other disorders.

Infections and accidents.

Nervous system.

Activity.

Habits.

Figure.

Digestion.

1

a

Childhood.

Adult.

Wasser-
mann test.

Alcohol.

Tobacco.

Appetite and
diet.

Bowels.

25

Jew.

yrs.
50

Housewife.

Erysipelas twice; apo-
plexy twice.

-

Rather nervous.

Ordinary.

Normal.

Obese.

Good.

Constipate(

26

M.
F.

American.

14

Schoolgiri.

Several re-
mote rela-
tives.

Maternal grand-
mother, cancer.

Men si es ; whooping-
cough; chicken-pox.

Nervous; slight
chorea.

a

Much candy.

Thin.

it

It

27

n

42

Clerk.

Sister, cardiorenal.

Measles; chicken-pqx;
diphtheria; mumps
(orchitis).

Jaundice; appendicitis;
malaria; sore throats.

Normal.

it

Little.

Moderate.

No excess.

Normal.

a

Regular.

28

(I

11

Schoolgirl.

Paternal
granduncle.

Whooping-cough; mea-
sles; chicken-pox;
mumps; poliomyeli-
tis (?).

Choreiform move-
ments.

Studious.

a it

it

it

it

29

Finn.

26

Domestic.

Two sisters;
brother.

Whooping-cough.

Hemoptysis.

Normal.

Ordinary.

Starch, not
sugar.

it

it

Constipate

30

it

American.

45

Housewife.

Usual (indefinite).

Typhoid; grippe; appen-
dicitis (operation) ;
menorrhagia (curet-
tage); mastoiditis (op-
eration).

Nervous.

a

Moderate.

Moderate.

Simple.

Slightly
obese.

Poor.

Regular.

31

M.
F.

it

35

Real estate
agent.

Father, sarcoma.

Measles; whooping-
cough.

Gonorrhea; rheumatism;
chorea; sore throats.

Normal.

a

Little.

it

Normal.

Normal.

Good.

Constipate

32

Jew.

21-

Housewife.

Diphtheria; measles;
pneumonia.

Tonsillitis.

Nervous.

it

ii

Starch, not
sugar.

it

it

tc

33

li

51

li

Sister.

Measles; typhus.

Acute nephritis following
colds.

it

a

Much starch
and sweets.

Obese.

Occasional
indiges-
tion.

it

34

M.

ti

26

Clerk.

Mother; sis-
ter.

it

—

Normal.

ti

Little.

Moderate.

No excess.

Normal.

Good.

ti

35

American.

61

Lawyer.

Cousin, cancer.
Father, para-
lytic condition.

Grippe; measles; mumps;
whooping-cough.

a

Healthful.

ti

Normal.

it

i(

Regular^

36

it

ti

30

Engineer.

Sister; cousin.

Mother, myxe-
dema. Father,
Bright's disease.

Measles; diphtheria.

Digitized

Peritonsillar abscess; ne-
crosis of jaw; septi-
cemia.

Dy IVIicrosoft®

Nervous.

Ordinary.

Little.

it

a

it

li

a

TABLE 1— Continued.

Past history.

Diabetic history.

Activity.

Habits.

Figure.

Digestion.

Bowels.

Onset.

Glycosuria discovered.

Weight.

Polypha-
gia.

Polydipsia

and
polyuria.

Pruritus.

Skin infections.

Albuminuria.

Menstruation or
sexual function.

Pains.

Alopecia.

A

ystem.

Alcohol.

Tobacco.

Appetite and
diet.

Acute or
gradual.

Date o£ first
symptoms .

Time.

Cause of examina-
tion.

Highest.

At
onset.

At
admis-
sion.

Degree.

2 «

rvous.

Ordinary.

Normal.

Obese.

Good.

Constipated.

Gradual.

1911

1911

Routine.

kg.
96

kg.

84.5

kg.

76

-

-

■'

Slight.

Normal till cli-
macteric.

Entire body.

Heavy.

+

slight

it

Much candy.

Thin.

ii

u

Acute.

Feb., 1913

Mar., 1913

Polyphagia;
polydipsia;
loss of weight
and strength.

31.2

+

+

Moderate 1st
admission;
negative sub-
sequently.

Stopped Feb.,
1913.

Moderate.

Moderate.

u

Little.

Moderate.

No excess.

Normal.

ii

Regular.

Gradual.

1907

1907

Dental caries;
infection of
mandible.

59.6

Carbuncle.

Retained.

Slight.

ii

a move-

Studious.

ii it

11

ii

ii

Acute.

Jan., 1915

Jan., 1915

Polyuria.

29

+

+

Ordinary.

Starch, not
sugar.

a

ii

Constipated.

a

1915

1915

Weakness; poly-
phagia; poly-
dipsia.

52.5

45.6

+

+

Normal.

Slight.

it

Moderate.

Moderate.

Simple.

Slightly
obese.

Poor.

Regular.

it

June, 1914

Oct., 1914

Pruritus; poly-
phagia; poly-
dipsia.

73

57

56.8

+

+

Vulvar,
marked.

Faint.

ii

Marked.

Heavy.

i(

Little.

it

Normal.

Normal.

Good.

Constipated.

Gradual.

1912

1912

Debility.

68.4

53.4

Incipient gan-
grene of toe.

Great toe.

SUght.

ii

U

a

Starch, not
sugar.

ii

11

11

Acute.

June, 1914

Oct., 1914

Amenorrhea.

53.2

+

+

Vulvar,
marked.

Faint 1st 15
days.

Stopped Oct.,
1914.

a

+

it

Much starch
and sweets.

Obese.

Occasional
indiges-
tion.

i{

Gradual.

i

1912

1912

Nervousness;
lassitude;
pains.

96

83

Faint 1st 15
days.

Normal till cli-
macteric at
50.

Head; limbs.

Moderate.

Insignificant.

ti

Little.

Moderate.

No excess.

Normal.

Good.

it

u

Nov., 1911

Oct., 1912

Pain in arms.

51.6

+

+

Slight.

Moderate 1st 3
days.

Libido lessened.

Arms.

Slight.

Heavy.

Healthful.

i(

Normal.

a

it

Regular.

it

1904

1905

Backache; poly-
uria.

66.4

a

Ordinary.

Little.

u

ti

u

a

(C

Acute.

Dec, 1913

Jan., 1914 Polydipsia; 64
polyuria; loss
of weight.

Digitize i by Microsou®

50.2

+

Colon bacillus
wound infec-
tion; abscess-
es on neck.

Heavy at 3rd
admission.

Absent.

Moderate.

ii

Physical examination.

Menstruation or
sexual function.

Pains.

Alopecia.

Acidosis.

Complexion.

Nutrition.

Thyroid.

Teeth.

Tonsils.

Heart.

Lungs.

Liver.

Lymph glands.

Knee jerks.

Blood
pressure.

250

.So

Remarks.

inuria.

Degree.

s 1
S.3

+

Hyperp-
nea.

Digestive
symptoms.

Normal till cli-
macteric.

Entire body.

Heavy.

Atypi-
cal.

Vomiting.

Cyanotic.

Obese.

Normal .

Marked caries
and pyor-
rhea.

Hypertrophied ;
no pus foci.

Hypertrophied.

Emphysema;
bronchitis.

Edge felt at costal
margin.

Normal.

Absent.

110
70

Left hemiplegia; beginning atyp-
ical coma; fecal retention.

te 1st
sion;
ive sub-
itly.

Stopped Feb.,
1913.

Moderate.

Moderate.

-

Sallow.

Emaciated.

a

Good.

Normal.

Normal.

Normal.

Normal.

it

Normal.

105

Retained.

Slight.

"

"

a

Fair.

ii

Many missing;
caries; pyor-
rhea.

it

it

it

Edge felt at costal
margin.

it

Large carbuncle on neck, with
fever.

Good.

Good.

a

Good.

Hypertrophied;
no pus foci.

it

it

Normal.

Slight epitrochlear
enlargement.

Exaggerated.

90

85

75

Normal.

Slight.

-

"

"

Poor.

Fair.

it

ti

Normal.

it

it

it

Slight axillary en-
largement.

Active.

110

Tuberculosis not demonstrated.

ii

Marked.

Heavy.

Fair.

Slightly
emaci-
ated.

it

it

it

it

Edge felt at costal
margin.

Slight axillary and
epitrochlear en-
largement.

Sluggish.

110
90

Fasting acidosis.

-

Great toe.

Slight.

li

"

"

SaUow.

Emaciated.

it

it

a

a

it

Normal.

Axillary palpable.

it

Arteries palpably sclerotic.

1st 15

Stopped Oct.,
1914.

a

+

+

Good.

Good.

it

Slight caries;
pyorrhea.

Hypertrophied;
pus exuda-
tion.

it

it

ti

Axillary and epi-
trochlear en-
largement.

Absent.

100

6b

Tonsillectomy performed later.

1st IS

Normal till cli-
macteric at
50.

Head; limbs.

Moderate.

Insignificant.

"

"

ii

Obese.

ii

All missing.

Normal.

Slight murmur.

Emphysema.

it

Normal.

Exaggerated.

190

100

Trace of albuminuria.

te 1st 3

Libido lessened.

Arms.

Slight.

Heavy.

-

—

—

High.

Thin.

it

Good.

it

Normal.

Normal.

it

a

Normal.

110

90

~

it

Ruddy.

Fair.

it

ii

it

a

it

Edge felt 4 cm.
below costal
margin.

Slight axUlary and
epitrochlear en-
largement.

Sluggish.

120

80

at 3rd
ission.

Absent.

Moderate.

a

Sallow.

Thin.

" Impacted wis- "
dom root.

Digitized by Ivlicrosoft®

it

it

Normal.

Normal.

Normal.

100

00

Diabetes dating from sepsis.

General data.

Family history.

Past history.

6

z;

Sex.

Nationality or
race.

Age.

Occupation.

Diabetes.

Obesity.

Tuberculosis.

Other disorders.

Infections and accidents.

Nervous system.

Activity .

H abits.

Figure.

Digestion.

Bowels.

P

Childhood.

Adult.

Wasser-
raann test.

Alcohol.

Tobacco.

Appetite and
diet.

A

37

M.
F.

ii

M.

American.

yrs.
16

Schoolboy.

Measles; chicken-pox.

Alveolar abscess; severe
cold.

-

Normal.

Healthful.

Normal.

Normal.

Good.

Regular.

A(

38

Jew.

39

27

Housewife.

Brother.

Visceroptosis.

n

Ordinary.

Little.

it

a

13

39

American.

Teacher.

Mother.

Father and broth-
er nervous. Ma-
ternal grand-
father, cancer.
Paternal aunt,
insanity.

Scarlet fever and others.

Neurotic.

Hard mental
work.

it

Slightly
obese.

a

a

G^

40

i(

29

Doorman.

(Little known.)

Measles; whooping-
cough; scarlatina.

Gonorrhea; chancre;
colds.

Normal.

Ordinary.

Excess.

Moderate.

Small.

Normal.

Fair.

ii

Ae

41

Irish.

52

Politician.

Sister.

Insanity on moth-
er's side.

Measles; mumps; scarlet
fever; chicken-pox;
diphtheria.

Gonorrhea; syphilis; tu-
berculosis; grippe.

+ + + +

It

Checkered life.

Moderate.

a

Normal.

Slightly
obese.

Good.

ii

Ge

42

F.

American.

11

Schoolgirl.

Measles; whooping-
cough; scarlet fever.

Nervous.

Strain in school
work.

Small.

Normal.

((

ii

Aa

43

M.

i(

27

Nurse.

Maternal
aunt.

Maternal
grand-
mother.

Measles; mumps; whoop-
ing-cough; chicken-
pox; diphtheria; pneu-
monia.

Malaria; septicemia with
nephritis.

ii

Ordinary.

Normal.

a

ii

a

t(

44

n

53

Electrician.

Aunt, cancer.

Diphtheria.

Gonorrhea; colds; pleur-
isy with hemoptysis.

Moderately nerv-
ous.

it

Little.

Moderate.

Some excess
in sweets.

it

a

ii

Gh

45

££

Jew.

6

(Child.)

Paternal
great grand-
mother;
grandfather;
uncle.

Family slight-
ly obese.

Maternal grand-
mother, cancer.

None before diabetes;
grippe and otitis media
after.

Normal.

Healthful.

Much sweets.

a

u

Constipated.

Aci

46

<f

i(

48

Storekeeper.

Daughter.

Pneumonia. Double inguinal hernia. —

Digitized by IVIicroson®

it

Sedentary,

Moderate.

Moderate.

No excess.

it

u

((

(C

TABLE— I Continued.

Past history.

Diabetic history.

Activity.

Habits.

Figure.

Digestion.

Bowels.

Onset.

Glycosuria discovered.

Weight.

Polypha-
gia.

Polydipsia

and
polyuria.

Pruritus.

Skin infections.

Albuminuria.

Menstruation or
sexual function.

Pains.

Alopecia.

Nervous system.

Alcohol-

Tobacco.

Appetite and
diet.

Acute or
gradual.

Date of first
symptoms.

Time.

Cause of examina-
tion.

Highest.

At
onset.

At
admis-
sion.

Degree.

[ormal.

Healthful.

Normal.

Normal.

Good.

Regular.

Acute.

Mar., 1915

Mar., 1915

Polydipsia; poly-
uria; weak-
ness; drowsi-
ness.

kg.
55

kg.

kg.
47.4

-

+

-

Heavy.

iC

Ordinary.

Little.

a

a

ti

Unknown.

Mar. 20,
1915

Hospital rou-
tine.

Slight.

Pregnant.

ti

"eurotic.

Hard mental
work.

a

Slightly
obese.

u

ti

Gradual.

1910

1910

Headache; poly-
dipsia; poly-
uria.

85

59.2

+

Vulvar,
slight.

" with
coma.

Stopped Mar.,
1915.

■

Intense facial
neuralgia.

Moderate.

Moderate.

'ormal.

Ordinary.

Excess.

Moderate.

Small.

Normal.

Fair.

it

Acute.

Apr., 191S

Apr. 12,
1915

Hospital rou-
tine.

45.4

Heavy 1st 10
days.

Heavy,

It

Checkered life.

Moderate.

i(

Normal.

Slightly
obese.

Good.

ti

Gradual.

1911

1911

Routine.

86.5

83

+

+

Ulcers on shins.

Slight.

Normal.

Present, not
due to dia-
betes.

Slight.

"ervous.

Strain in school
work.

«

Small.

Normal.

a

it

Acute.

Feb., 1915

Feb., 1915

Polyphagia; poly-
dipsia; poly-
uria.

26.8

+

+

Terminal with
coma.

Beginning.

Moderate.

a

Ordinary.

Normal.

a

ti

ti

it

Jan., 1915

Mar., 1915

Polyphagia; poly-
dipsia; poly-
uria; loss of
weight.

54

44

44

+

+

Vulvar,
marked.

Trace for 1st
few weeks.

Stopped.

Marked.

it

[oderately nerv-
ous.

((

Little.

Moderate.

Some excess
in sweets.

a

it

it

Gradual.

July, 1914

Apr., 1915

Pleurisy; poly-
dipsia; poly-
uria.

77

73

62

+

Cramps in
legs.

Slight.

Heavy.

ormal.

Healthful.

Much sweets.

a

it

Constipated.

Acute.

Nov., 1914

Nov., 1914

Polyuria; loss
of weight.

21.6

16.4

19.4

+

Incipient gan-
grene over
sacrum.

Marked.

it

Sedentary,

Moderate.

Moderate.

No excess.

u

ti

it

Oct., 1914 Oct., 1914 Acute thirst.

Digkized b)\ Microsof\®

68

51.2

+

Back and
legs.

Present, not
due to dia-
betes.

it

Physical examination.

Menstruation or
sexual function.

Pains.

Alopecia.

Acidosis .

Complexion.

Nutrition.

Thyroid.

Teeth.

Tonsils.

Heart.

Lungs.

Liver.

Lymph glands.

Knee jerks.

Blood
pressure.

inuria.

Degree.

s.s

Hyperp-
nea.

Digestive
symptoms.

.a

5
90

90

7'0
70

Remarks.

-

Heavy.

+

+

-

High.

Fair.

Normal.

Caries; pyor-
rhea; alveo-
lar abscess.

Hypertrophied;
pus foci pres-
ent.

Normal.

Normal .

Normal.

Slight general
adenopathy.

Active.

120'

Received with impending coma.

Pregnant.

a

+

+ ■

Flushed.

Good.

a

Missing.

Normal.

ii

Lobar pneu-
monia.

Edge felt 3 cm.
below costal
margin.

Normal.

Absent.

150

Admitted on pneumonia service.
Otitis media; pericarditis;
pregnancy; artificial delivery;
diabetic coma.

1

Stopped Mar.,
1915.

Intense facial
neuralgia.

Moderate.

Moderate.

Good.

Fair.

Possible
slight en-
large-
ment.

Slight caries;
pyorrhea.

Normal.

Normal.

a

Normal.

125

Mentally irresponsible at times.

1st 10

Heavy.

+

Cyanotic.

u

Normal.

Many missing;
caries; pyor-
rhea.

a

ii

Lobar pneu-
monia.

11

Slight epitrochlear
enlargement.

Active.

Admitted on pneumonia service.
Hematuria; diabetes transi-
tory.

Normal.

Present, not
due to dia-
betes.

Slight.

^

"

Good.

Slightly
obese.

a

All missing.

Slightly hyper-
trophied; no
pus foci.

11

Bronchitis; em-
physema.

11

Slight adenopathy.

Normal.

125

Luetic.

1 with

Beginning.

Moderate.

Vomiting.

i(

Good.

li

Good.

Hypertrophied,
with pus foci.

11

Normal.

11

A few palpable.

a

Tuberculosis later developed.

or 1st
ieks.

Stopped.

^

Marked.

li

+

Pale.

Poor.

11

it

Normal.

li

a

li

11 li li

ii

62

Tendency to edema.

Cramps in
legs.

Slight.

Heavy.

Fair.

it

li

Many missing;
moderate ca-
ries; pyorrhea.

ii

a

li

li

Slight adenopathy.

ii

90

Cough and night sweats preced-
ing admission; tuberculosis not
demonstrated.

li

Pasty.

Emaciated.

a

Spongy, bleed-
ing gums.

li

it

Hydrothorax.

li

Normal.

Absent (?).

62

Extreme bicarbonate edema; al-
kalosis; nephritis; diabetic
coma.

Back and
legs.

Present, not
due to dia-
betes.

It

Pale.

iC

" Many missing; "
caries; pyor-

Digitized by Microsoft®

Hypertrophied.

Normal.

ii

Slight general
adenopathy.

It

Very feeble appearance; slight
arteriosclerosis.

General data.

Family history.

Past history.

d

Sex,

F.

M.

F.

Nationality or
race.

Age.

Occupation.

Diabetes.

Obesity.

Tuberculosis.

Other disorders.

Infections and accidents.

Nervous system.

Activity.

Habits.

Figure.

Digestion.

Bowels.

1

(5

Childhood.

Adult.

Wasser-
mann test.

Alcohol-

Tobacco.

Appetite and
diet.

Acute
gradu

47

American.

yrs.

31

Saleswoman.

Maternal
grand-
mother.

Usual.

-

Normal.

Ordinary,

No excess.

Normal.

Good.

Regular.

Gradr

48

ii

20

Clerk.

Two uncles.

None remembered.

Sore throats; dental
caries.

Degenerate.

it

Moderate.

Excessive.

it it

Thin.

C(

if

Acute,

49

iC

30

Seamstress.

Measles; mumps; chick-
en-pox; scarlet fever;
diphtheria.

Tonsillitis; two high for-
ceps deliveries.

Nervous.

it

it it

Normal.

i(

It

il

SO

M.
F.

a

11

54

Teacher.

Usual.

±

ii

it

it li

it

il

a

Gradual

51

a

7

Schoolboy.

Whooping-cough.

—

Normal.

it

it ti

it

ii

it

Acute

52

ii

27

None.

Measles; chicken-pox.

i(

it

tt it

ti

ii

ti

Gradual

53

ii

9

Schoolgirl.

Measles; mumps; chick-
en-pox; tonsillitis;
slight rheumatism.

Nervous.

it

a it

It

ii

it

Acute,

54

a

ii

29

Telephone op-
erator.

Measles; whooping-
cough.

1 miscarriage.

Normal.

it

Normal.

ti

it

Constipated.

ii

55

M.

ii

26 mos.

(Infant.)

Paternal great
grand-
mother.

it

it

it

tt

ti

Regular.

11

56

a

30

Clerk.

Maternal aunt, in-
sanity. Two
sisters, rheuma-
toid arthritis.

Whooping-cough; gastro-
intestinal attacks;
swollen cervical glands;
enuresis.

Grippe preceding dia-
betes.

it

it

Moderate.

Some excess
in sweets.

Thin.

it

Constipated.

a

57

Jew.

37

Physician.

Mother; ma-
ternal uncle;
maternal
aunt; sis-
ter.

Family obese.

Paternal aunt,
cancer. Father
and mother,
first cousins.

Measles. Jaundice; tonsilhtis. —

Digitiied by Microso ^®

Somewhat nerv-
ous.

it

Moderate.

Excess in
food,
sweets,
and coffee.

Obese.

it

Regular.

ti

TABLE— I

Continued.

history.

Diabetic history.

Habits.

Figure.

Digestion.

Bowels.

Onset.

Glycosuria discovered.

Weight.

Polypha-
gia.

Polydipsia

and
polyuria.

Pruritus.

Skin infections.

Albuminuria.

Menstruation or
sexual function.

Pains.

Alopecia.

Acidosis.

Alcohol.

Tobacco.

Appetite and
diet.

Acute or
gradual.

Date of first
symptoms.

Time.

Cause of examina-
tion.

Highest.

At
onset.

At
admis-
sion.

Degree.

It

Hyper-
pnea.

Digestive
symptoms.

U

No excess.

Normal.

Good.

Regular.

Gradual.

1911

1911

Pruritus vul/£e;
polyphagia;
polydipsia;
loss of weight

ki.
84

kg.
66

67.3

+

+

Vulvar,
marked.

Superficial,
vulvar.

-

Normal.

Heavy.

-

-

-

Hi

Moderate.

Excessive.

a u

Thin.

H

((

Acute.

1914

1914

Polyphagia; poly-
dipsia; poly-
uria.

45

+

+

it

+

Pa

li It

Normal.

li

a

a

June, 1914

Dec, 1914

Polyphagia; poly-
dipsia; poly-
uria; loss of
weight.

68

52.4

+

+

Trace at first.

Normal.

Slight.

a

i

a u

i(

it

11

Gradual.

1912

1912

Polyphagia; poly-
dipsia; poly-
uria.

49.6

+

+

Stopped at on-
set of present
illness.

Universal.

Moderate.

Moderate.

+

Vomiting.

11 u

it

a

i(

Acute.

Oct., 1914

Oct., 1914

Coma.

18.3

+

+

Trace at admis-
sion.

li

~

"

V(

a ti

a

i(

ii

Gradual.

1911

1911

Lassitude.

58

48.4

SKght.

Stopped June,
1915.

Slight.

Heavy.

P£

li a

u

a

it

Acute.

1913

1913

Polyphagia ; poly-
dipsia; poly-
uria.

20

+

+

Vulvar.

a

Normal.

iC

n

Constipated.

i(

June, 1915

July, 1915

Polydipsia; poly-
uria; loss of
weight and
strength.

65

49

+

+

Normal.

it

+

a

a

a

Regular.

(f

Oct., 1915

Oct., 1915

Polyphagia; poly-
dipsia; poly-
uria.

113.5

11.8

+

+

li

+

v\

Moderate.

Some excess
in sweets.

Thin.

It

Constipated.

a

1912

Jan., 1913

Weakness and
depression.

51

+

+

Stopped.

Slight,

a

p

Moderate.

Excess in
food,
sweets,
and coffee.

Obese.

ic

Regular.

it

1899
1907

1899
1907

1899, accidental.
1907, furuncu-
losis.

88 86.2 + +

?c/ Dv Microsoft®

SUght.

Numerous boils
and ulcers.

Lessened.

Moderate, not
evidently
due to dia-
betes.

Slight.

!•'

Physical examination.

Menstruation or
sexual function.

Pains.

Alopecia.

Acidosis.

Complexion.

Nutrition.

Thyroid.

Teeth.

Tonsils.

Heart.

Lungs.

Liver.

Lymph glands.

Knee jerks.

Blood
pressure.

nuria.

Degree.

s.s

Hyper-
pnea.

Digestive
symptoms.

„d

M

60

Remarks.

Normal.

Heavy.

-

-

-

High.

Good.

Normal.

Slight pyor-
rhea.

Enlarged; no
pus foci.

Normal.

J

Normal.

Normal.

Slight axillary en-
largement.

Normal.

90

it

-1-

Pale.

Emaciated.

ii

Fair.

Normal.

ii

ii

ii

Normal.

it

Very inferior type.

first.

Normal.

Slight.

a

i{

Poor.

ii

a

ii

ii

ii

a

it

it

Transitory dimness of vision;
cold and fever at admission.

Stopped at on-
set of present
illness.

Universal.

Moderate.

Moderate.

+

Vomiting.

" sallow.

Fair.

a

Many missing;
caries; pyor-
rhea.

a

ii

ii

Edge felt If cm.
below costal
margin.

it

90

75

Myxedema, treated with thyroid
feeding.

admis-

i(

—

—

—

Very pale.

a

a

Good.

it

ii

ii

Normal.

it

it

Apparently very acute onset.

Stopped June,
1915.

Slight.

Heavy.

^

Pale.

a

Slight en-
large-
ment.

ii

Slight hyper-
trophy; no
pus foci.

ii

a

ii

Slight axillary and
epitrochlear en-
largemOit.

ti

"

ii

Emaciated.

Normal.

"

Normal.

ii

ii

ii

Normal.

it

Appears constitutionally feeble.

Normal.

li

+

+

a

Fair.

a

a

a

ii

ii

a

li

Sluggish.

110

80

Progressive downward progress.

It

"

Flushed.

it

a

ii

Hypertrophied;
slight exuda-
tion of pus.

li

a

Slight epitrochlear
enlargement.

Normal.

Stopped.

Slight,

It

Pale.

Emaciated.

ii

Some caries.

Normal.

ii

ii

a

Slight adenopathy.

Diminished.

100

80

Lessened.

Moderate, not
evidently
due to dia-
betes.

Slight.

Florid.

Obese.

" Marked caries
and pyor-
rhea.

Digitized by M

Greatly hyper-
trophied.

crosoft®

ii

ii

Edge felt at costal
margin.

Moderate anterior
cervical enlarge-
ment.

Sluggish.

120

85

Hj^eridrosis with diabetes.

General data.

Family history.

Past history.

1

Sex.

Nationality or
race.

Age.

Occupation.

Diabetes.

Obesity.

Tuberculosis.

Other disorders.

Infections and accidents.

Nervous system.

Activity.

Habits.

Figure.

Digestion.

Bowels.

Onset.

.a

0

Childhood.

Adult.

Wasser-
mann test.

Alcohol.

Tobacco.

Appetite and
diet.

Acute or
gradual.

Date
syn

58

F.
F.

American.

yrs.

72

Housewife.

Whooping-cough.

-

Normal.

Ordinary.

Little.

Normal.

Slightly
obese.

Good.

Regular.

Gradual.

June

59

46

Physician.

Maternal
aunt.

Father, cancer.
Mother, gout
and rheuma-
tism. Sister,
"acidosis."

Measles; whooping-
cough; scarlet fever;
gastrointestinal at-
tacks; sunstroke.

Albuminuria; sciatica;
gout; axiUary abscess;
boils and carbuncles.

Nervous.

Intellectual
overwork.

Moderate.

Excess

No excess.

Thin.

Rather
poor.

a

iC

Pert
18

60

a

43

Housewife.

Whooping-cough; mea-
sles; cMcken-pox.

"Gastric fever;" tonsil-
litis.

Normal.

Ordinary.

Normal.

Normal.

Good.

iC

Acute.

Apr

61

M.

F.
M.

\ "

17

m7

30

Papermalier.

Father, rheuma-
tism. Mother
paralysis.

Diarrhea; scarlet fever;
rheumatism.

Measles; mumps (orchi-
tis); rheumatism; trau-
ma of elbow.

i{

Heavy lifting.

Excess.

a

it

a

iC

Gradual.

June

62

((

19

None.

Maternal
grand-
mother.

Whooping-cough; mea-
sles; chicken-pox; dia-
betes (?).

it

Easy life.

No excess.

Thin.

Acute.

it

63

Polish.

13

Schoolboy.

-

Measles; chicken-pox;
scarlet fever.

tc

Ordinary.

it it

Normal.

a

i(

a

Feb.

64

Jew.

12

a

Measles; mumps; fall on
head.

ti

Healthful.

Normal.

a

n

a

65

American.

53

Business.

Father.

Brother, Hodg-
kin;-.' disease.

Measles ; diphtheria ;
"gravel."

it

Ordinary.

Little.

Excess.

it

Slightly
obese.

a

Gradual.

Oct.

66

ti

IS

Schoolgirl.

Paternal
grandfather.

Tonsillectomy; measles;
urticaria.

—

ti

Healthful.

it

Normal.

a

a

Acute.

it

67

Spanish.

46

Merchant.

Maternal
aunt; pater-
nal cousin.

Usual; mild.

Syphilis.

+ +

Nervous.

Business strain.

Considerable.

Considerable.

Large.

i(

it

a

Gradual.

Dec.

68

Jew.

23 mos.

(Infant.)

Maternal
great grand-
mother and
grand-
mother.

Slight colds; vaccination. — Normal,

Digitized by IVIicrQsoft^

Normal.

Normal.

a

iC

i(

Acute.

May

TABLE I—

Continued.

Diabetic history.

Habits.

Figure.

Digestion.

Bowels.

Onset.

Glycosuria discovered.

Wciglit.

Polyplia-
gia.

Polydipsia

and
polyuria.

Pruritus.

Skin infections.

Albuminuria.

Menstruation or
sexual function.

Pains.

Alopecia.

Acidosis.

cohol.

Tobacco.

Appetite and
diet.

Acute or
gradual.

Date of first
symptoms.

Time.

Cause of examina-
tion.

Higliest.

At
onset.

At
admis-
sion.

Degree.

1.1

Hyperp-
nea.

Digestive
symptoms.

Complexion

•

Normal.

Slightly
obese.

Good.

Regular.

Gradual.

June, 1911

June, 1911

Failing vision.

kg-

kg.

kg.

68

-

+

Ulcers of foot.

Very faint.

Normal till cli-
macteric.

Insignificant.

-

-

-

Pale.

rate.

Excess.

No excess.

Thin.

Rather
poor.

ii.

{(

Perhaps
1889

1910

Polyuria.

52.6

Boils and car-
buncles.

Diminished.

Sciatica; gout.

Present, not
evidently
due to dia-
betes.

Moderate.

ii

Normal.

Normal.

Good.

a

Acute.

Apr., 1915

June, 1915

Loss of weight;
polydipsia;
pruritus vul-
v«.

78

36.6

+

+

Vulvar,
marked.

Stopped 1915.

Moderate.

Heavy.

+

+

ti

Excess.

n

"

u

Gradual.

June, 1915

1915

Polydipsia; poly-
uria; weakness.

74.0

+

Slight.

a

Slightly cy
anotic.

No excess.

Thin.

iC

f.i

Acute.

1911

1911

Polydipsia;
polyTiria.

52.2

39.4

-1-

+

" 1912.

Heavy.

Flushed.

a it

Normal.

a

a

ii

Feb., 1915

Feb., 1915

Polydipsia;
polyuria; loss
of weight and
strength.

27.8

-f

+

Faint 1st 10
days.

a

+

+

Very pale.

Normal.

it

li

1916

1916

Polydipsia;
polyuria.

25.2

+

Faint at admis-
sion.

i<

-1-

+

Flushed.

Excess.

11

Slightly
obese.

li

u

Gradual.

Oct., 1915

1916

Loss of weight.

61.1

Cramps in
legs; head-
aches.

Not due to
diabetes.

Good.

it

Normal.

u

a

Acute.

1915

1916

Polydipsia.

50

+

—

Stopped Dec,
1916.

Trace.

"

"

"

Healthy.

derable.

Considerable.

Large.

a

u

Gradual.

Dec, 1913

Dec, 1913

Feverish sensa-
tion.

90

85

54.2

Diminished.

Headaches.

Not due to di-
abetes.

Shght.

ii

Normal.

it

u

a

Acute.

May, 1916

June, 1916

Poljrphagia;
polydipsia;
polyuria; in-
cipient coma.

11.3 9.1 8.5 + +

Digitized by Microsoft®

Slight at first.

Heavy.

+

4-

Flushed.

Physical examination.

Menstruation or
sexual function.

Pains.

Alopeda.

Acidosis.

Complexion.

Nutrition.

Thyroid.

Teeth.

Tonsils.

Heart.

Lungs.

Liver.

Lymph glands.

Knee jerks.

Blood
pressure.

a.

Degree.

s.a

Hyperp-
nea.

Digestive
symptoms.

U3

A .a

S2

Remarks.

Normal till cli-
macteric.

Insignificant.

-

-

-

Pale.

Good.

Normal.

All missing.

Normal.

Normal.

Emphysema.

Edge felt 4 cm.
below costal
margin.

Normal.

Normal.

185

120

Double cataract and diabetic
retinitis.

Diminished.

Sciatica; gout.

Present, not
evidently
due to dia-
betes.

Moderate.

li

Emaciated.

u

Slight pyor-
rhea.

a

it

Normal.

Normal.

Slight general
adenopathy.

it

118

88

Insurance refused for albumi-
nuria in 1899.

Stopped 1915.

Moderate.

Heavy.

+

+

a

a

it

Good.

Hypertrophied;
no pus foci.

It

ii

It

Normal.

Absent.

ii

Slightly cy-
anotic.

Good.

tc

Several miss-
ing.

Normal.

Arrhythmia;
hypertrophy;
mitral regur-
gitation and
stenosis.

a

it

a

Active.

160

120

Admitted on cardiorenal service.
Valvular disease; chronic in-
terstitial nephritis.

" 1912.

Heavy.

Flushed.

Emaciated.

ii

Caries.

Slightly en-
larged; pus
on pressure.

Normal.

ii

Edge felt at costal
margin.

ii

Normal.

Pneumonia subsequently under
treatment.

10

a

+
+

+

Very pale.

Moderately
emaci-
ated.

ii

Good.

Normal.

ii

ii

Normal.

it

Sluggish.

Received in coma.

lis-

ii

+

Flushed.

Moderately
emaci-
ated.

ii

Poor; moder-
ate pyor-
rhea.

Moderate in
size; pus on
pressure.

li

a

ii

Slight general en-
largement.

it

Received in incipient coma.

Cramps in
legs; head-
aches.

Not due to
diabetes.

■

Good.

Good.

ii

Good.

Normal.

C(

u

Edge felt at costal
margin.

Normal.

Normal.

160

80

Stopped Dec,
1916.

Trace.

—

—

—

Healthy.

<(

it

a

Missing.

t(

ii

Normal.

it

li

90

60

Diminished.

Headaches.

Not due to di-
abetes.

SUght.

u

Poor.

it

Much caries;
marked py-
orrhea.

Normal.

li

a

ii

Slight inguinal en-
largement.

Absent.

Troublesome insomnia; lues.

Heavy.

+

+

Flushed.

Fair.

Good.

Dicitized by

Hjrpertrophied; "
no pus foci.

MicrosofifE)

i(

it

Slight cervical and
axillary enlarge-
ment.

Normal

Received in incipient coma.

General data.

Family liistory.

Past history.

1

Sex.

Nationality or
race.

Age.

Occupation.

Diabetes.

Obesity.

Tuberculosis.

Other disorders.

Infections and accidents.

Nervous system.

Activity.

Habits.

Figure.

Digestion,

Bowels.

1

S

Childhood.

Adult.

Wasser-
mann test.

Alcohol.

Tobacco.

Appetite and
diet.

Acute or
gradual.

69

F.

M.

il

F.

Jew.

yrs.
39

Housewife.

Father, Bright's
disease. Moth-
er, cancer. 2
brothers, paral-
ysis.

Usual.

"Vaginal cellulitis"
twice; 5 abortions.

—

Very neurotic.

Worried, hectic
life.

Moderate.

Restrained.

Tendency
to obes-
ity.

Good.

Regular.

Acute.

70

American.

34

Physician.

Mother, tumor
and Bright's
disease.

Measles.

Normal.

Easy, quiet life.

Little.

Little.

Normal.

Normal.

iC

a

a

71

9

(Child.)

u

Normal.

a

a

ii

a

ii

72

a

12

Schoolgirl.

Measles mumps; chick-
en-poj.

ti

it

ti

it

a

Constipated.

'(

73

a

ti

3

(Child.)

Paternal
grandfather.

—

it

ti

'*

a

ii

Regular;

ii

74

M.

li

23

Plumber.

—

It

ti

Moderate.

a

a

a

a

a

75

Canadian
(Irish).

33

Teamster.

Measles; Humps.

iC

ti

Some excess.

Considerable.

li

ti

ii

ii

li

76

a

American.

4

(Child.)

Maternal
grandaunt;
cousin.

Whooping-(ough; otitis
media.

DinH-i

.«./K\

It

it

it

it

li

a

i(

UlylLl^cu uy iviii^iuouw'i:^

i

TABLE 1— Concluded.

Past history.

Diabetic history.

Activity.

Habits.

Figure.

Digestion.

Bowels.

Onset.

Glycosuria discovered.

Weiglit.

Polyp Iia-
gia.

Polydipsia

and_
polyuria.

Pruritus.

Skin infections.

Albuminuria.

Menstruation or
sexual function.

Pains.

Alopecia.

Acidosis.

Alcohol.

Tobacco .

Appetite and
diet.

Acute or
gradual.

Date of first
symptoms.

Time,

Cause of examina-
tion.

dighest.

At
onset.

At
admis-
sion.

Degree.

ii

2.S

Hyperp-
nea.

Worried, hectic
life.

Moderate.

Restrained.

Tendency
to obes-
ity.

Good.

Regular.

Acute.

Dec, 1915

Jan., 1916

Polyphagia;
polydipsia;
polyuria; loss
of weight and
strength.

62.8

kg.

58.6

kg.

37.0

+

+

Extreme.

—

Stopped.

Head and
limbs.

Marked.

Heavy.

+

—

Easy, quiet life.

Little.

Little.

Normal.

Normal.

a

a

Sept., 1914

Sept., 1914

Polydipsia;
polyuria.

60.0

59.0

42.2

+

ii

Progressing.

ii

Normal.

a

i(

u

a

Oct., 1914

Oct., 1914

Polyphagia;
polyuria.

14.8

+

+

Trace.

ii

+

a

a

a

a

Constipated.

ii

Nov., 1915

Nov., 1915

Lassitude.

31.6

—

—

" at 2nd
admission.

ii

-

+

ii

a

a

"

Regular.

ii

Dec, 1915

Dec, 1915

Polydipsia; loss
of weight.

9.8

—

—

—

Insignificant.

i(

Moderate.

a

u

"

a

'^

Jan., 1916

Feb., 1916

Polydipsia;
weakness.

63.8

43.6

—

+

—

Heavy.

+

it

Some excess.

Considerable.

a

a

a

li

ii.

June, 1914

1914

Polydipsia;
polyuria; loss
of teeth.

59.2

37.6

+

Stopped.

Moderate.

Slight.

i(

a

li

li

ii

ii

Feb., 1917

Mar., 1917 Polyuria.

Dfaitized bv

15

Microsoft®

+

i(

Physical examination.

Menstruation or
sexual function.

Pains.

Aiopecia.

Acidosis.

Complexion.

Nutrition.

Thyroid.

Teeth.

Tonsils.

Heart.

Lungs.

Liver.

Lymph glands.

Knee jerks.

Blood
pressure.

Degree.

a.s

Hyperp-
nea.

Digestive
symptoms.

70

.So

50
65

Remarks -

Stopped.

Head and
limbs.

Marked.

Heavy.

-

-

-

Sallow.

Very emaci-
ated.

Normal.

Normal.

Nonnal.

Normal.

Normal.

Edge felt 2 cm.
below costal
margin.

Slight general en-
largement.

Normal.

Highly hysterical

a

Progressing.

a

+

Pale.

Very emaci-
ated.

it

Gums reced-
ing.

a

" action
weak.

i(

Normal.

Normal,

Absent.

85

it

+

a

Moderately
emaci-
ated.

K

Gums reced-
ing.

it

Normal,

a

a

it

a

Received in coma.

nd

it

-

+

—

High.

Fair.

((

Poor; pyor-
rhea.

a

a

i(

it

it

Feeble.

" with impending coma.

Insignificant.

—

—

Pale.

Emaciated.

a

Good.

it

a

a

it

ii

Absent.

Very feeble; chronic pot-belly.

Heavy.

+

—

U

it

a

Fair.

a

a

a

it

ii

a

Tuberculosis subsequently.

Stopped.

Moderate.

Slight.

Weather-
beaten,
yellowish.

it

i(

All missing.

a

a

li

ii

it

it

110

80
70

it

Pale.

Good.

Good.

Digitized hy Microsoft^)

li

■ii

Axillary and epi-
trochlear pal-
pable on both
sides.

Active.

90

CAJENaE,204 raTcom

BIET

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<S^Jl ,i^ AO«U<T itntHKX 0«yo8E» KOVEHSBR

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KAY iTONE JULY AUS04T SESTETTOES, QCTQ-BES. KOVEMBtt lECEMBEi

2 29 1 a 5 7 9 a a 15 17 19 81 83 25 2789 81-1 3 5 7 9 11 « 15 tt 19 S 23 25 EI 23 1 » 5 7 9 11 13 15 17 19 21 2S !S H 29 3H 3 5 7 9 0 IS SS 17 !9 21 2S 25 272931-1 3 5 7 9 11 a,15«19a23 25SJ291 J 5 7 91iai5H19E183 25 27 29 5M S 3 7 911U15H19a232SH89 1 S ! 791113 IS 17)9

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MAY

30NW

AO(iUST

itmnvBR

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HOV&HBGK

Chart 2. Case No. 1.

Digitized by IVIicrosoft®

KCmBSK

Date.

Glucose

excreted in

24 hrs.

Date.

Glucose
excreted in

24 hrs.

iPJ-#

gm.

1914

itit.

Feb. 24

27.0*

July 22

3.8

" 25

86.6

" 23

6,0

" 26

58.2

" 24

1.5

" 27

27.3

" 26

8,8

" 28

3.8

" 28

9.3

Mar. 7

1.2

" 29

28,0

" 9

3.0

" 30

0,8

" 10

15.0

" 31

3,7

" 11

9.0

Aug. 1

7,8

" 12

33.8

" 2

5.2

" 13

23.0

" 3

0,5

" 14

22.0

" 4

0.1

" 15

38.4

" 10

0,4

" 16

3.0

" 13

0,4

" 19

16.2

" 30

4.4

" 21

1.7

« 31

2.3

" 22

3.5

Sept. 1

0,9

" 31

1.4

" 2

0,6

Apr. 12

0.4

" 3

0,3

" 13

0.4

" 4

0,6

" 15

0.1

" 7

0.5

" 17

0.3

" 8

11,7

" 18

0.2

" 9

8.0

" 21

2.0

" 10

9,7

" 22

5.1

" 11

1,5

" 23

12.1

" 12

1,9

" 24

7.3

" 13

0.8

" 29

1.3

" 14

1.2

" 30

4.1

" 15

3,4

May 1

1.7

" 16

1,3

June 4

1.8

" 27

1,4

" 20

8.9

Oct. 1

2,4

" 24

6.0

" 26

1,1

" 28

3.3

Nov. 14

1,4

July 1

4.1

" 15

3,2

" 2

7.1

" 20

2,0

" 3

14.6

" 21

5,8

" 4

4.0

" 30

1,9

" 12

9.6

Dec. 2

2,8

" 13

5.5

" 5

3,9

" 14

7.4

" 12

6,5

" 20

3.3

" 13

3,2

12 hr. specimen.

30UY WT.
KILOS

(•ii

41
39

/?.

1,600
1,400
1,200

1,000
800

600
^00

zoo

. 0

Htia ruACsi

SUCHTB MOCB

3,500
I ti. 3.000

ri.UID.| |WTAK£ ^000

OUTfOT 1,500

1,000

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AFRll. MAT JOHB JotY AUSUjT

lOABMissioK 1914 » 15 IT 19 a a » KM i i s t 9 n c is b a a a zs a a 31-1 a 5 7 9 11 b s g 19 a ts ts n aa 1 a 5 ? 9 11 s 15 g s a as 85 27 ^^ ^" ^ Jj' ^ " J^ a-ABMissioN '=^' "•'■'''" "

BIET 100

IN CAUOS.IE3 800

0 WHISKY 300

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tAftBOHY!mATE5oo

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U TAT aoo

900

1,000

1,100

1,800

1,J00

1,400

fia 1,500
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TOTAL N J la iVoo

«ft M HR5A a 1^300

4 1,900

I O S,00O

2,100

2,200

2,300

2,400

JATibAiCf ISlS
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25 27 29 M-1 3 5 7 9 11 13 » IJ 59 21 23 2

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9 . U U t$ 17 1* » 83 ir 27 !19 1 3 J 7

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Chart 3. Case No. 2.

11 13 15 17 lSaMasn29»J 3 J 7.9 « » ai719 21 23 2I»7J» jw J V.'A

Di^ftizea by Microsmm

11 » 1; 17 13 21 23 2317 23 1 3 ! 7 9 U U 15 17 19 21 21 25 27 2»a-] II I 9 It J3 IS » 19 81 23 25

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Date.

Glucose

excreted in

24 hrs.

Date.

1st admission.

2nd admission.

3rd admission.

* 17 hr. specimen,
t 14 "

Glucose

excreted in
24 hrs.

1914

gm.

1914

gm.

Apr. 13

31.0*

June 22

16.9

" 14

36.0

" 23

22.9

" IS

SI. 9

" 24

19.8

" 16

78.0

" 25

19.6

" 17

51.6

" 26

19.5

" 18

42.5

" 27

28.6

" 19

31.7

" 28

24.9

" 20

5.0

" 29

29.0

" 21

O.S

" 30

34.6

" 24

1.9

July 1

32.9

" 25

0.7

" 2

20.7

" 26

3.1

" 3

37.9

May 22

3.8

" 4

13.0

June 4

12.2

" 5

3.6

" 5

2.0

" 6

1.0

" 20

7.9

" 21

21.4

1915

Dec. 14

7.7

Apr. 1

0.1

" 15

0.8

" 2

3.0

" 26

3.0

" 18

5.6

1915

May 28

5.8

Jan. 11

2.9

Sept. 2

2.2

" 21

1.0

1916

" 28

2.4

Jan. 6

53.6

Feb. 13

2.2

" 7

42.5

" 24

0.4

1916

1916

Mar. 20

38. 3t

June 7

45.0

June 6

51.0

CASE NO. 1^162,

1914 '

D1£T
IN tALOMES

■dUNE dULY AUaUaT ^tPTEMBER OCTODtR.

«Z52ri9t S S 7 9 II 13 15 17 19 2123^5 2729 3H 3 5 7 9 1113 151719212325272931-13 S 7 9 11 l» 15 17 1921 23252729 13 5 7 9 U 13 15 17 19

-■ -' . ■ = = = = = = = = =HB±± = = = = = = = aa = = = = B = -^- = alll.lllllaM«« = Ha=2 = -

PER.
24HR3.

ACEToks ECI»e£

3,500

llNTAK-E 2^00

FLUID'^ 2.000

a 1,500

aOWTPUT j,000

5(

an

too

SltT

200

IBMI-OME*

300

400

SOO

600

700

SOO

900

1,000

1,100

1^200

1,300

1,400

1,500

EO

1,000

16

GM

1,700

12

L TOTAI. N

1,800

0

7ER 24 HRS.

1,900

4

2,0004^0 J

2,100

2,200

2,300

2,400

fBODrWT.OM

dc-H Total

ACITONS SomES

eC^NHj

NEdLD TRACE S
aU6)1TB MOD. a
iiEAVYB

QQwmwnv& a

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JONE JULY AU«Ui£T «EPTEM!ER 0W06BR

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"^ART 4. Cas/No. 4.

3,500 ^ >,

3,000

2,500 INTAKEIUi;;,^
2,000 7

1,500 OUTfUTBJ
ifiOO
500
o

nek i"'"''^

Date.

Glucose
excreted in

24 hts.

/»/■?

Sm.

June 22

39.2*

" 23

42.5

" 24

32.6

" 25

13.0

" 26

6.8

".; 27

16.3

" 28

8.9

" 29

1.2

July 23

1.4

" 30

0.4

Aug. 6

0.4

" 7

0.7

" 8

0.6

" 10

0.1

" 20

3.7

" 21

2.8

" 22

2.2

Sept. 1

0.7

" 2

0.5

" 3

46.2

" 4

3.9

" 10

0.3

« 11

0.5

" 12

1.8

« 13

4.4

" 14

14.3

" 15

15.4

" 16

3.2

" 17

1.7

" 18

0.5

" 23

0.8

" 26

0.7

12 hr. specimen.

Ca:»E m. 2,169

JULY
laADKlSAIOM 1914 15 1719 21^3

DIET

■WHISK.Y
IcAaBOHYDnKTE

i vo-oruti

D TAT

AUaUST ;SET>TEMtbEH. OCTOBER KOYI.J»iCiJa

25 27 29 3H 3 S 7 9 11 13 15 17 19 2123 25 27 29 31-1 3 5 7 9 11 13 IS 17 19 21 23 2527 29 1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 3M 3 5 19

■PIVL
24 HRS. ■<

ILUID'

SUSHTD MOO. Bl01liJlE-|
HEAW ■ I

QTJAMTltftTWE HJ

1915

JMATiMJSSlOH

'i:r

15 17 « 21 M SJ S7 1? Jl-J

iSPTajjm^n

Chart

Digitized by Microsoft®

IRT 5. Case No. 5.

100
20O
300
400

soo
600
700

soo

900

1,000

1,100

1,200

],soo

1«00
1,500
l,6O0
1,700
1,300
1,900
2,000
2,100
2,200
2,300
2,400

11IE.Y

utcxumts

*> rBOttfVT.ON
j3 UVDMIS5I0N

57

55

l,60<r
1,400
1,?00
1,000

600
600
•400
2 00
4-0

CClgroTAU
AcvioKi wtres

Cti

3,S00

3,000

2,S00 INTAK-eI

2,000

OOTPUll

1,*00

1,000

JOO

o

Date.

Glucose

excreted in

24 hrs.

1st admission.

1914

gm.

July 15

40.0*

" 16

32.3

" 17

60.8

" 18

10.2

" 19

2.9

" 20

1.6

Sept. 17

3.0

" 18

2.7

" 19

6.7

" 20

14.5

" 21

54.4

" 22

124.2

" 23

102.0

" 24

50.9

" 25

168.7

" 26

202.8

" 27

36.3

13 hr. specimen.

>nuii>

CA5E,Na ^134-

JWY AUGUST
IQl'*' H«27«9 3J-1 3 5 7 9» ii 15 iri9 21 2i 25

IN CAl-QNCS
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Date.

Glucose

excreted in

24 hrs.

in4

fm.

July 25

59.9

" 26

34.3

" 27

30.7

" 28

98.0

" 30

112.7

" 31

24.5

PAug. 1

8.7

^1" 2

2.4

TIDIB

a a 27 J9 «-i 3 f T 9 a is ir n 15 v

JULY ADSU5T

Chart 6. Case No. 6.

neb /

1914

mCALOOEf

X)LY Jffl(xU3T SEPTEMBER OCTOSER. KOVETOtS. BECE^!BE^ JWJUAKriSlS TEWUARY

E9 311 3 5 7 9 11 13 15 17 19 a 23 Z! 27 29 31-1 3 5 7 9 U 13 15 17 19 21 23 85 27 29 1 3 5 7 9 11 1315 a B 21 2S 25 27^9 31-1 3 5 7 9 11 13 15 IT 19 H 23 25 2T 29 1 3 5 3 9 n tt i; 17 19 21 23 25 27 29 31-1 3 5 7 9 B 11 iS 1? » 21 li !S 27 29 ^M 3 5 7 9 U 13 li 17 19 II M 85 'I 1

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BLOOD SUMS.
PER CENT

f "•
J i INTAKE

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51ISHTB MOIXB
HEWYH
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Chart 7. Case No. 8.

J ff 7 9 11 13 15 17 » 21 J3 25 27 29 3U 4 J 7 S » 13 15 " 19 2J 23 « 27 29 3H J r 7 9 11 !3 IJ 17 19 Jl 23 25 27 1 3 J 7 » Jl U U 17 19 21

MKOARV J315 fE8it.UM-( JIAMH

J3T SEPTEMBER OCTOBER.

7 9 11 » 15 n 19 a 23 25 27 29 311 3 5 7 9 11 B 15 17 » 21 23 B5 27 Z9 1 3 5 7 9 11 » 15 1

KOVEHBER.
B 21 ?5 25 2719 iH 3 3 7 9

BECEMBES. OKNOMnr J9IS TEWUARY >1.ASCH

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Date.

Glucose

excreted in

24 hrs.

Date.

Glucose

excreted io

24 hrs.

1914

gm.

ISIIS

gm.

July 28

44.2*

Jan. 2

1.0

" 29

61.6

" 3

1.3

" 30

65.0

" 8

4.7

" 31

58.2

" 9

5.0

Aug. 1

60.6

" 10

5.0

" 2

17.8

" 12

11.4

" 3

1.9

" 13

15.3

" 4

2.0

" 14

23.0

" 20

0.4

" 15

12.2

" 30

6.6

" 16

43.8

" 31

8.1

" 17

44.4

Sept. 1

0.8

" 18

46.0

" 9

1.3

" 19

69.6

" 10

1.0

" 20

76.2

" 11

3.2

" 21

60.8

" 12

0.4

" 22

16.0

" 13

1.1

" 23

8.1

" 14

3.2

" 24

33.7

" IS

2.3

" 25

47.3

" 16

1.7

" 26

44.4

" 26

1.6

" 28

60.0

" 27

1.5

" 29

67.4

Oct. 26

1.1

" 30

49.4

" 27

1.8

" 31

42.5

Nov. 3

2.8

Feb. 1

16.5

" 9

5.4

" 2

8.2

" 10

3.7

" 3

6.8

" 14

1.5

" 4

2.8

" 15

2.4

" 10

1.5

" 20

1.8

Mar. 12

10.6

" 21

9.0

" 13

2.2

Dec. 2

5.7

« 14

7.3

" 12

1.5

" 15

18.6

" 13

1.7

" 16

22.2

" 14

4.4

" 17

33.2

" 15

1.1

" 18

62.9

" 19

21.8

" 19

64.9

" 20

8.5

" 20

84.9

" 22

0.6

« 21

54.4

" 28

0.5

" 30

0.5

" 31

3.5

rLoiD

* 12_hr. specimen.

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TOTM.N

Date.

Glucose

excreted in

24 hrs.

1914

Sm.

Oct. 7

45.4*

" 8

79.4

" 9

77.3

" 10

75.6

" 11

98.0

" 12

J6.7

" 13

7.0

" 14

3.4

Nov. 12

1.0

" 13

2.7

" 14

3.2

" 15

3.2

" 16

0.5

" 28

8.5

Dec. 7

6.8

" 8

12.5

" 9

0.9

1915

Jan. 6

4.8

" 9

3.7

" 10

10.2

■ 14 hr. specimen.

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Date.

Glucose

excreted in

24 hrs.

1st admission.

1914

««.

Nov. 11

42.4*

" 12

26.0

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6.9

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0.8

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Chart H- Case No. 13.

OCTOBER KCWEMRER
Kf JOTIE OtroiER HOVEJMIR IICEWSER -WW 1916 25 27 29 31.1 1 k ? q >i ., it r>

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19 21 23 25 27 29 1 3 S 7 9 U B IS 17 19 21 23 25 27 29 311 3 S 7 9 II 13 IS 17 19 21 23 25 2J 29 3H
I>E<iEHBEE JANUARY 1917 TEB.

Chart H- Case No. 13.

Digitized by IVIicrosoft®

Date.

Glucose

excreted in

24 hrs.

1st admission.

1914

gm.

Nov. 14

66.7*

" 15

46.8

" 16

2.2

" 17

1.1

" 18

0.5

" 20

0.3

" 30

0.1

Dec. 3

1.2

" 7

0.1

" 9

1.8

" 14

3.7

mis

Jan. 31

1.4

Mar. 7

4.6

" 8

0.7

May 28

6.4

3rd admission.

July 7

6.4t

* 13 hr. specimen.
tl3i "

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1914

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Date.

Glucose

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24 hrs.

1st admission.

1914

Nov. 20
« 21

gm.

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Jan. 25
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3.2

2.S

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1914

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Glucose

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24 hrs.

/Pi4

«»>.

Nov. 28

29.2

" 29

17.0

Dec. 2

9.1

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10.6

" 5

1.4

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6.S

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1.2

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3.6

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2.3

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2.3

191S

Jan. 26

1.5

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1915 II 19 21 25 25 21 29 3U 3 3 7 9 U 15 15 17 19 a j

a"'AI)Ml«ION

as I 3 S J 9 11 13 IS 17 19 21 83 a 27 » 3H 5 5 7 9 H IS IS 17 19 21 J3 25 O 29 3H 3 5 7 9 II IS JS m» 21 !3 !S !J 1 3 5 7 9 « 13 IS 17 19 81 ij If S7 29 311 3 5 T 9 U 13 15 H 19 21 23 jr 27 29 1 3 S 7 9 11 13 JS 17 19 21 23 JS 27 29 JH 3 S 1 9 II 13 » 17 19 21 8J 25 2T

KOY. DECEMbER JAKUARYISJS TtBROAKf MARCH A-PRll. MATT OVWE

n 19 21 23 2S 22 29 )H 3 S 7 9 It 13 IS 17 19 21 »

OCTOBER NOVEMBER

Digitized by IVIicrosoft®

Chart 20. Case No. 24.

TEaP-UAKV MARCH APRIL MAV (JONE

21 »iS a 29 31-1 3 5 T 9 (I IS 15 IT 19 21 iJ 25 21 1 3 5 T 9 U 15 15 K 19 U 2S 25 2l 29 31-1 3 S ? 9 U 13 W B 19 21 23 2J 2? 29 1 3 5 1 9 U 13 15 17 19 a a 25 27 29 Jl-1 3 5 7 9

U B IS ir 19 21 25 25 2r

■^ ■<'^QnDa-i'ia'^-^'^'^-^'^'<'«iinB'^-<tBBBBB-^n

1915

17 19 21 25 25

KOYtZABEK
2: 29 3H 3 5 7 9 U 13 15 17 19

21 23 25 2729-1 3 5 7 9 11 13 15 IT 19

JANUARY 1916
21 23 25 27 29.3H 3 J I 9 11 13 15 17

I 21 23 25 n 29 SM 3 J t 9 U 13 IS 17 1» 21 S3 SJ 2J I 3 S 7 9 H 13 IS 17 19 81 23 IS J7 29 MI 3 S J 9 U 13 15 17 » 2) 23 JS 27 89 1 3 S 7 9 31 13 IS 17 19 21 23 25 27 29 «1 3 I J 9 11 13 m7 19 21 83 25 2T
TSBRUASJ MARCH A7R1I. _ HAY JV»K

» 19 81 23 2S 28 24 )M 3 S 7 9

OCTOBER NOVEHBtK

1-IW»W I I I I I I I I I I I I I l»l»l IW I I I I I I I I I I I I I I I I 11*1 I I I 1 I I

n 13 II IJ 19 81 M 2S 27 29 1 3 S 7 9 1] 13 IS « 19 81 23 2S 27 29 311 3 J 7 9 1113 IS 17
l)ECS«a2R MHOARY 1916

lOO SIEl

iOO IR CAIORIE*

30O

400

500

600

roo
eoo

900
1,000
1)200
1,200
l,S0O
1,400
l.SOO
1,£00

i.roo
i,aoo

1,900

Z,ooo

2,100

ZiZOO

i.300 r LoWtn LIMIT OP

MOO J NonMAL TLASHA

l^ roR Coa

Date.

Glucose

excreted in

24 his.

1st admission.

19H

gm.

Nov. 28

46.0*

" 29

45.0

" 30

20.5

Dec. 2

4.5

" 3

2.7

" 10

9.9

" 11

20.4

" 12

5.7

" 15

2.6

" 16

2.7

191$

Jan. 10

0.7

Apr. 23

6.6

" 24

2.7

4-i-
48

ftiOIKWr.OM
*"t ADMISSION

10 hr. specimen.

-40
a«
36

IjSOO"
1,400

Voo

1,000

600

600

400

200
♦-0-'
0400
0.350
0.300
0.2$0
0.200

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3,50Q

3,000 .

2,500 JNTAKElUryu,
2,000 >»1.WJ»

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1,000
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O

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TtClj J

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Chart 20. Case No. 24.

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CAX NO. 2,255

mAWUSSIOH

19M

vcsr
mCKxsiixti

100
200
800
B WHISKY ^00

I CftRBOHYSRATE 500

a 600

H yROTEIN
D TAT

NOV. CC^EMStX JAXtUOY 1915 TEStagm rSSSUAKY /USCH

29 1 3 5 7 9ai3J5»»a23MCT»SH S S 7 911S3Mn»a!3aa aS»i 3 5 7_ 1915 n B IS JI 19 a S3 JS 17 1 S S 7 9 Jl 13 H 17 19 !I S3 !S

mmmmmmmimimsi^mumMmmmmmmmmimm

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COMBtWH* WITH

lOOtt. ^

BLOOD TIASHA

700

600

900

l,0OO

1,10°
1,400
1,300
1,400

^0 1,500

16 1,600

18 1,700

a 1,800

■» 1,900

O tfiOO

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25

76
7-*

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10

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1,600

1,400

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600

600

400

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NOV. SECEKSaH JANtSAKY 1915 TtWSJAXt

1 eo DIET

JOO ™ CAIOWM

30O
400
soo

600

roo

800

900

1,000

1,100

l,20O
1,300
1,400

1,500 ^o•^

1,600 16 ^_

1,700 izLtomlN

1.800 8 f ygJJ „^^.

1,900 4

Date.

Glucose

excreted in

2 4 hrs.

1st admission.

1914

«<B.

Nov. 28

10.0*

" 29

14.3

" 30

4.5

Dec. 13

2. '2

" 16

1.2

" 17

1.1

2^ao«-oj

i" lowTs LIMIT or
NORMAL fLASH^
tOKBINIHS ?0W1»

feoDY «XON
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3,500

3,000 CO.

2.500 iNTAirall
2,000

1,500 ootkjtSI

1,000 '

500

PIUIJ)

n 13 15 n IS a 83 !i 21 1 a s 2 9 11 13 is ij is a i% is

* 18 hr. specimen.

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CASE no.

iVAstrassan

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IH CM.afatS

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ZXQO

■StCtMKR JvOiOAKY 191S nSKViHt MARCH iQir

_ ^^ 2'»AvniumM

100 ' """ """' ■-—'—'''■" - '

zoo

300

OCTOBUR NOVIMBER HXeEMBEK UNO/UtY 1916 TEBISIARY

5 7 9 n 15 15 17 19 M 23 S3 21 Z9 SH 3 5 7 9 U » IS 17 19 21 25 25 27 29 1 5 5 7 9 n n « 17 J9 21 24 25 B S 311 » 5 7 9 n B 15 17 19 21 23 25 2T 29 SW 3 5 7 9 11 a 15 U la a 23 il

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Chart 22. Case No. 26.

"^ -stctmitft jAHOARTr 191S nmnacf «arcb

SON 1914 7 9U13 15Xri9 2I292S:r29iM 9 S 7 9UU15ffl9»i325rT29a'l S t 7 9Il]S1!1719!13SZ5ni 9 S

ocToBtR NovrHBtR «CEM»E» oMiaMtrisie rmmoaw

1915 5 7 9 n IS 15 17 19 a 23M n 29 3H 3 5 1 9 11 B 15 17 19 11 J! 25 27 SS 1 5 5 5 9 n B 15 17 J9 21 2S 25 iJ » 311 » 5 7 9 D O 15 O 19 21 23 25 27 2» SH 3 5 7 9 «

J5 17 » Zj 23 25

I 9 i: » IS >7 19 U u 25 » 2«

OTCmSM

Chart 22. Case No. 26.

100 vtr

too isewiBES

too

400

500

eoo

700
SOS
900

i,ooe
1,100
l,eoa

j;>oo

1,400

1,S00

1,000
1,70a

1,000
1,000

a^ooo

2,100
2,100

V"" riOW»l.IMITOF

^l*? J HO«HM. TLMtlA

L roRO%
( ton WTOH

Sl*~ J^ AtMSSOM

29

87

25

V>oa
l,soo

],OO0

800
600
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20O

o

0.400
O.S50

0.300
asso

O.20O

O-lSO MOXMAU

0.100 ■«- 51005 sus.^A

0.0S0

0,500

3^000 cc.

"i^" intaklI'stloi6

2,000 . /

,^00 OUTPUT Bl
1,000
soa
O

DEXTKMI
HCI3

I'

UNHt

Date.

Glucose

excreted in

24 hrs.

1st admission.

1914

««.

Dec. 7

44.5*

" 8

14.3

" 9

9.9

" 10

6.8

" 11

S.5

1915

Feb. 27

5.9

" 28

7.6

Mar.. 3

1.2

" 4

0.3

16 hr. specimen.

•^ S^"^ JA-HOKSN PEB2U«W

1915 15 17 19 a 23 25 zr 29 31-1 3 5 7 9 U 13 15 1? 19

DIET
IK CALORIES

S WHWKY

ICAMOHYDSATS
§ PROTEIH
D EST

coMBiHiNS wira^ 43

lOOCC. \
■bLOODPlflSHA

3,500
3,000
2,800.
2,000
1,500

1,000
TOO

23 a E7 1 3 5 7 9 U 13 15 1! 19 a 23 25 Zr 29 3M 3 S 7 9 11 13 15 17 19 21 25 25 27 29 1

Date.

Glucose

excreted in

24 hrs.

i!ii5

gm.

Jan. 15

36.4*

" 16

32.4

" 17

9.7

" 18

6.6

* 12 hr. specimen.

GH.

TSRMHllS.

iOWERUHlTQP

CoHauutrefovjER.

feoiW WT.OH

0.1 00 .«_

0.050

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I N iiiTOu I iirii H I HI iiHH iiii ! Hi I! li irHiiiiH MiiTim'iimiiinwiii^'ri'i

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« 12 19 11 25 a a w 3M 3 5 7 9 M IS 15 17 19 a 2S 2S 2J 1 3 S 7
WHUART rEBRUATlY

9 11 U IS 17 13 21 23 iS 27 :9 Sl'l 3 S ! 9 IS » 15 n IS 21 23 IS 21 29 1

3,500

3,000 '^'•

2.500 INTAKtllTLura

2,000

1,500 OliTT-OTB

1,000

500
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Chart 23. Case No. 27.

CAStH0.ZZ79

*>-"- » .w^*-' MNUAW TEBRXWKT

la/amsssBK 1915 sajjKwasH 3519

JHtAlOBW goo
WmSKY *°°

ei.oT6oj

100 Ct. ■^■'5
BLOOti fLASMA

KEA □ TRACE a
JUSHTB MOT>. B
HEAVY"
QOANriTATIYE S

3915

>JOYS^ER OT<E«BE».

2,900 /•t.oWMt UMITOP
2,400 J KOMAL yiJiSMA
*^^eo«8tNIK4 POWEE
I FOR tot

Jtbodv wt. on

lADMISSION

Jiiiiiniir ;>;

riwiTiiii

lll-iKiSnriiM

!i!iiii!h

ACIC

8oo^<it-t5«Ha

600

100 C<!.9«BSA

Joo

♦-0 J

KORHAL
BLOOD i^lSAIt

a,soo

3,000
2,800
^''> UJTAKtl,

I 000 OW"' B

■nuiB

M-l joo
0

sbmtrm;

n ai »^ »s n 19 Ml 3 s 7

,1 ]3 15 )J !9 M « 25 M 1 3 i'
MARCH

u n IS n » n 23 a 27 » 1 3 s 7 9 ii « is n »

BBICTRllJCl

aiUKE

KOVSXStK

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CASINO. S,32-4

1315

5 5 7 9 11151517 19 21212527 1

3 5 7 9 1115 151719 2125 2527 29 31-1 i 5 7 9 U 13 iS 17 19 21

B1E.T
JN CALOEILS

OCOFCOg

COMBININ* WITH •{

100 ei.

liooi) PLASMA

JLUIB

.SUtSKTB

QUANHTATIVEB^

TRAttEM r-

3,500
3,000
IlNTAKS. 2,500
2,oco

1,500 |-
1,000

500
0
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50E tOi

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Date.

1915
Jan. 27
" 28

Glucose

excreted in

24 hrs.

7.5*
2.1

12 hr. specimen.

27 29 Sl-l 3 S 1 9 U 13 J5 S7 19 U » :; » 1 3 5 I 9 11 13 IS 17 19 U »><» 29 31-1
JAN. FEBRUARY J^KRCK

»rZIROSE'\ _

f 7

APR5L

9 11 iJ If II J9 21

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100
200
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1400
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i ■PROTEIN

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INCALOKIES

CCoFCOg

CQHfilNiNe vnrn 4
too cc

(MOD TIASMA

«$

55

■45

3S

-V.

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25
CCg NHj

CC^UREA

nvm-

Date.

Glucose

excreted in

24 hrs.

1915

im.

Feb. 3

5.5

" 7

10.1

" 8

*

* Incontinence of urine.
Unable to collect spec-
imen.

iOWEP. LIMIT Of
NORMAl. PLASMA
ConDUHNSfOWUt
lOB cog

. ^BOWfWT.ON
' *T. ADHISSIOW

IIl«.a IKACEG
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2,000

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S,SOO
3,000
2,S00

2.000 nnwt

J,500

i^oe aarfna

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Chart 26. Case No. 30.

CASE NQ 2^89

f/OHissJOH 1935

•MET lOO

mOttOMM '"O

300

WHISKY 400

mV^AKf AlAHtH AFjai, /<lAlr JOKS JULY

ISJ5 17i9!lM25 2ri S 579 II 13 15 nSJl 23 iS 17 29 31-1 3 5791113I5n:9 2in«na9J SJ79U»35 1JSaS3 2J2?»3HS579I113 15ns212325 2?291 3 57 1915

liiii:iiiiiIiiiiil^iii=ni:::iiliii;iiliiiiiilHU^nH=i=diiiui|||iiiilllilEiliiiiiiliH

DZt. ifHOAXt 191«
29 31-1 3 5 7 9 « 13 15 17 19 M 23

ecorfot
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rioro

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MM
IN CALO«IE$

i' towGR imrror
KORKAL PUUMA
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TOR COi

iSOBT WT.ON
ATiniSjION

9 Jl !3 IS n IS Jl !J 2J 27 « 31-

17 19-21 23 2J 27 19 1 3 5 7 ? 11 IJ IS 17 S II 23 2f J7 29 JH 3 5 7 9 11 13 IS 17 19 il 23 81 fJ » J 3 S 7

Digitized by IVIicrosoft®

Chart 27. Case No. 31.

Date.

Glucose

excreted in

24 hrs.

1st admission.

H 1015

gm.

Feb. 12

48.6*

" 13

31.3

« 14

1.4

" 25

0.1

Mar. 5

0.5

« 13

5.3

« 14

2.3

* 18 hr. specimen.

NOKMAL
BLOOS ja«AR

*<*"'» iktakeII „„
)T1.0JB

UxmE

29 3H 3 S 7 9 11 13 15 17 IS SI 23
SSC. JANUARY 1916

CASE wo. 2,312_,

£,DnUABY f\mcil APmi. ,n. ,

liVHJ-HJilOM J.y 'i5 IS 21 23 25 27 1 3 S 7 9 U 13 15 17 19 21 232S272951-1 3 5 7 9 1915

DILT J 00

IN CALORiLS 200

VK15K.Y 300

8 400

CARBOHYDRATE 500

PBOTElti 800

700

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Glucose

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;P75

gm.

Feb. 18

39.6*

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34.2

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10.7

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CASENQE^41

i3Ai>«iSsioJj 1915

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WtT

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Feb. 19

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CfaART 30. Cde No. 34.

JEfTEMBER

OCTOBER

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/Pi5

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Feb. 20

21.0*

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25.0

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22.0

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ISAWUSJION 1915

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Chart 32. Case No. 36.

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JULY
a iStn 7S 1 3 5 5 9 II D 15 n 19 »73 25

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Glucose

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iP/5

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Mar. 19

71.3*

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52.6

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36.2

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23.7

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9.0

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11.9

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2.6

3rd admission.

Feb. 19

20. 3t

' 20

99.9

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87.0

' 22

79.0

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102.9

' 24

67.9

' 25

59.0

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53.8

' 27

48.1

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28.6

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35.8

Mar. 1

23.9

Apr. 22

23.7

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10.5

* 12| hr. specimen.

tl4i "

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Chart 33. Case No. 37.

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Chart 37. Case No. 42.

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Date.

Glucose
excreted in
24 hours.

1st admission.

1915

«»«.

Oct. 27

6.S

Dec. 17

6.7

2nd admission.

May 6
« 7

11. S

2.7

3rd admission.

May 16

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CASE NO. 2,419

VAtntssKH 1915

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PROTEIN
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TABLE XIII.

Body
weight.

Temper-
ature.

Diet.

Treatment.

Fluid
intake.

Urine.

Acetone bodies.

Blood.

Date.

Total
calories.

Protein.

Fat.

Carbo-
hydrate.

Whisky.

Calcium

car-
bonate.

Sodium
bicar-
bonate.

Volume.

Reaction,

Total
nitro-
gen.

NH3-N

Sugar.

D:N
ratio.

i

Sugar,

Plasma
sugar.

Corpuscle sugar.

Plasma
CO2.

Hemo-
globin.

Corpus-
cles.

Lipemia.

Remarks.

|S^

53.

H»^

1915

kg.

°F.

gm.

gm.

gm.

cc.

gm.

«».

cc.

cc.

gm.

gm.

gm.

gm.

gm.

gm.

percent

per cent

per cent

vol.
percent

per cent

per cent

Sept. 1

19.4

98.5
96.3

28

—

—

■ —

8

15

15

1094

1185

Acid.

4.74

0.14

12.9

2.72

1.61

9.19

10.80

0,333

0.400

0.263
(calc, 0.166)

73.5

90

30.2

++++

Urine from 4:50 p.m. Sept. 1 to 7 a.m. Sept. 2.

" 2

22.0

97.4
96.2

56

—

—

—

16

20

20

3850

1405

Alkaline.

4.08

0.26

6.3

1.55

0.91

3.46

4.37

—

—

—

—

—

—

—

" 3

21.3

98.8
96.9

42

—

—

—

12

—

—

801

1345

Acid,

—

—

+ +

—

+ + +

—

—

—

—

—

—

—

—

—

" 4

20.2

99.0
96.4

7

—

—

—

2

—

—

476

1345

i(

2.96

0.21

+

—

1.07

0.11

1.18

—

—

—

—

—

—

—

" 5

20.0

97.4
96.2

—

■—

—

—

—

—

—

190

1260

Neutral.

2.15

0.11

0

—

0.56

0.04

0.60

—

—

—

—

—

—

—

" 6

—

96.8
95.4

196.9

1.0

—

53.3

15

,

5

972

945-1-

i(

'

0

"

"

"

___

'~~

~~'

_

—

5 a.m. 10 gm, levulose in 100 cc. water by stomach tube.

10 gm, levulose in 100 cc. saline, subcutaneously.

6:50 a.m. 20 gm. levulose in 250 cc. saline, subcutaneously.

" 7

17.6

100.8
98.8

946

48.7

73.0

—

19

—

5

1029

1418

Alkaline.

—

—

0

—

—

—

—

—

—

—

—

—

—

—

Ferric chloride reaction negative.

" 8

17.2

101.1
99.8

994

44.7

81.2

—

16

—

—

908

625

Acid.

8.86

0.56

++

—

0.12

1.15

1.27

—

—

—

—

—

—

—

" 9

102.2
99.6

613

24.5

31.3

40.5

16

5

958

788+

i(

7.43

0.60

11.32

0.45

3.03

3.48

0.286
0.287
0.222

0.286
0.308
0.27

0.25
(calc, 0.286)

0.227
(calc. 0.217)

0.164
(calc, 0.151)

67.8
84.9
85.9

80
82
95

34.0

27.5
39.8

++++

+++

+

11 a.m. Blood taken.

Oatmeal 60 gm. between noon and 5 p.m.
9 p.m. Blood taken before transfusion,
9 " Injection 225 cc. citrated blood.

12 m. Blood taken.

" 10

—

98.4
97.0

126

—

—

—

36

—

—

518

409-J-

it

Alkaline.

—

0.32

0

—

—

—

—

—

—

—

—

—

—

—

" 11

102.0
98.4

443

39.8

22.4

20

16

1456

860+

(C

3.16

0.15 0 — + — — —

0.066

Digitized oy Ivlicroson©

0.059

0.064
(calc. 0.075)

71.5

94

38.5

Plasma
clear.

7:30 to 8:45, a,m, 150 cc, citrated blood injected. By mistake blood

not taken before transfusion,
8:45 a.m. Blood taken at end of transfusion.

CAJbtNO. 2,4^55

1915 1 3 5

IN tALORttS
WHISKY
I eAMOHYDRATE
PROTEW

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7 9 tl 13 15 WIS 21 2$ 25 27 29 1 3 5 7 9 U 13 13 IT 19 21 2525 21 293H S J 7 9 11 13 15

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1,500

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MET
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1915

Sept. 24
" 25

Glucose

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24 his.

gm.

27.75
2.77

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Chart 40. Case No. 46.

CASINO. 2,491

1915

o

7 9 11

CTOIbE-K,
15 15 17 192125 25 27 2951-1 3 5

BltT
IN CALOnltS

WHISKY „

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100 ce.

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24 HE5. ^

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7 8 1115 1517 1921252327291 3 3

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100 WST

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300

400

500

600

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600

900
1,000
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1,200
1,300
1,400
1,500
J,600
1,700
1,800
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*' ■*\AT)niS510H

Date.

Glucose

excreted in

24 hrs.

1915

Oct. 6

" 7

66.2*
61.7

19J hr. specimen.

Samb

•NORMAL
*ia.000 SU&AR

11 » IS n » u 23 u 27 a a-1

9 II 13 )i IT 19 21 23 25 27 2S 1

:l » 15 17 » 21

3,500
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Chart 41. Case No. 47.

CASE NO. 2,469

' ^ OtTOBBa NOVEMBER -jEe.

1915 9 n a :s J7 19 a 23 25 2» 293H 3 ? 7 9 11 » U W 19 ai a JS 2if S9 1 2

WET
INCALORKS

WHISKY

Icasbohydrayb

i FR-OTEIH
D T-AV

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3,500
4000
2,500
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1,500
1,000
500
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100
200
300
400

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900

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2,600

2,100

2,200

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/bowwkoM

Date.

1915

Oct. 8

Glucose

excreted in

24 hrs.

118.2*

* 19 hr. specimen.

Kss, D Trace, s]

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Chart 42. Case No. 49.

CA5Em2,5^5

VAovsaan 1315

OCTOBEK JiOV2M8El! OECMreER MNDARY t3J6

9 11 U IS tt S i1J3 2S 2? 29 3M 4 5 1 9 H 13 If H 19 M aa J5 2» 29 1 3 5 7 9 11 13 ir 17 B 21 23 W >f 29 3M 3 S 1 9 « IS

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9 11 15 IS n 19 21 23 Si 27 i9 3H 3 ! 7 9 11 IS » 17 19 21 13 2S !7 29 1 3 f ? 9 11 IS 15 17 JS 21 23 2f 27 « 311 3 S 7 9 Jl 13
OCTOIER NOUBMKE ■ , ■ , , . «■ JtCZmZR -, -^ 3/SNUAS.Y 19J6

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Chart 43. Case No. 50.

/-

DIET
l°OjNC«.0raES
zoo

100
400
500
600
700

eoo

900
1,000
1,100
1.200
1,300
1,400
1,500
1,600
1,700
1,600
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2,000
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L TORCO2

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4S
43

1,600

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400

200

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5935 II 13 IS IT 19 a 2J 45 27 29 31-1 35 rsUtSlSlT 19 21 25 2527 «9 1 3 5 T 9 U » 1517 19 21 2S 25 2T 29 31-1 3Sr9U15lSi719

OCIODER WOVfcfMlER DE.CU4BER dANUAKV. 1916 ,_ . JUNE OUW AUGUST

i3iD 27 29 1 5 5 7 9 U B 15 17 IS 21 25 25 27 29 3H 3 5 7 9 11 13 15 17

DIET ^00

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IN
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Ct. ;^UREA

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OCtOBSIi. NOVEHSW IICEjretH IWOAKt 5916

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Chart 44. Case No. 51.

l^.=si=iin£rn::Hlil=il=±±l=£ik£=li£=£=

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Kl^

100 W"

joo wcauaaw

300
400

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30HE JULY «<SUST

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Glucose
excreted in

24 hrs.

1st admission.

1915
Oct 27

gm.

7.6

WADWSSION 1915 15 17 19 21 23 t5 87 29 311 3 5 7 9 11 18 15 17 19 al M 15 M 29 J 3 S 7 9 H IS 15

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OCTOBER NOVEMBER JANUA

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OCTOBER. NaVEMBER.

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Date.

Glucose

excreted in

24 hrs.

2nd admission.

/Pitf

«m.

Jan. 5

7.6*

" 6

6.7

" 7

7.9

• 8 hr. specimen.

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Chart 45. Case No. 52.

CASE NO. 2,561

19:5

DIET "°

IN«AU)WES 2"°

E300
WHlSKf 400

loatOWIUlATB 500

§^00
FEOTXm 700

D TAT ^°°

90O

1,600
1,100
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OCTOBER KOYEKBEE J£CEHBIS JANDAKY 1916 FEBflOARY

15 ir 19 21 23 25 27 S9 31-1 J 5 7 9 11 1! 1! 17 19 21 23 23 » 29 1 3 S 7 9 11 13 IS IJ 19 21 23 2S ZT 29 31-1 S 5 I 9 U 13 IS « 19 21 23 25 !J 29 3H 3 5 7 9 11 13 15 17 19 21 23 25

cc.or coj

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400
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600
700
800
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300

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400

200
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JANUARY 1916

TEWWARY

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Chart 47. Case No. 54.

NOYEMlER lECEKlai J«10AWi916 TCBRaAW «AKH .WRll. JUJiy JUKE jiji,-;

27 29 SH 3 S 7 9 U a 15 ]J 19 a a 25 27 M J 3 5 7 9 11 13 » 17 » M O 25 27 » «1 3 5 7 9 11 13 IS 17 « 81 » 85 I* » 5H 3 J 7 9 a 13 15 17 S 21 M U O 2« S 5 7 9 1! 13 S 17 19 a 23 2S 27 M MI 3 5 7 3 11 M IS 17 19 21 23 2S 27 29 1 3 5 7 9 11 IS 15 17 » 21 23 25 £7 » Wl 3 5 7 9 U U IS JJ 19 « 11 J« S? 24 1 3 f 7 9 11 « 15 17

fiM.
TW24HIU.

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♦"SSVeMtiHiHC fmntL

Date.

Glucose

excreted in

24 hrs.

1916

gm.

Jan. 6

2.4

" 11

6.7

" 12

7.4

" 13

8.1

" 19

3.2

Feb. 9

5.5

" 10

4.8

May 8

4.5

" 9

6.0

" 10

8.0

" 11

3.9

June 26

17.3

" 27

21.6

" 28

23.9

" 29

15.8

" 30

18.8

July 1

24.7

" 2

29.2

" 3

25.8

" 4

32.8

" 5

18.8

" 6

23.0

" 7

20.3

" 8

34.5

" 9

37.7

" 10

18.7

" 11

1.0

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il.001 5USAR

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3,000 ,

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NOVSMBEK DECEMBER JANUARY 1916 XtWlUtKS KAtcH ArB.1l. .MAY JUNE ^^^

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CH.4RT 47. Case N

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600
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Glucose

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JPJS

?»».

Nov. 3

17.05*

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41.6

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9.57

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8.83

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3.33

It

4

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Chart 48. Case No. 55.

15 H » 81 n 23 !7 29 1 3 5

MAY

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1,000
500
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lUAHMWilON 1935

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WKKKY

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D TAr

100
200
300
400
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500

800
900

1,000
3,lO0
3,200
1,300
1,400
1,500
1,600
1,700
1,600
1,900
2,000
2,100
2,200
2,S0O
2,400

65

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Chart 49. Case No. 56.

CA^ENO.2,-487

WADHWilOJ) 1915

S 5 7 9 11 n 15 17 19 a iS ZS 27 59 1 3 5 7 9 U 13 15 « » 1916 H » M 83 a? a? Ml » 5 7 S 11 13 15 17 19 8183 W alM SH 8 5 T 9 11 13 If 17 19 »1 tt K it M 1 S

DECEMBER
7 9 U 13 IS n 19 21 23 2E 27 29 3i-

JANUARY
13 5 7

1917
9 II

SIET
IN tALORIES

WHISKY

TROTEIH
FAT

g">APRI53Ii5N

3,Soo

3,000

i.roo

2,000

1,J00

1,000

300

0

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500
600
700

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1,000
1,100
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1,400

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1,700 12 I TOTAL N

1,600 SfpERllHRS.

1,900 4

ifiOO^-oJ

2,100

2,200

2,300 , lowERtmrror

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ir 19 21 23 25 27 2M 3 r 7 9 11 13 IS 17 19 U33 aS tl_» SM 3 I 7 9 U » IS )7 » » 11 it >7 t« 1 5
TCTROARt MAMH APRIL

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Chart 49. Case No. 56.

7 9 11 13 15 17 19 21 23 zr 27 2931-1 3 5 7 9 11 13 15 17 19 21 23 25 2J 29 3H 3 5 7 9 H 13 15 17 19 21 23 25 27 I 3 S 7
JAHUW0fl9l7 rEBRXIAKY KARCH

SXTROSE^

rtck

trWNE

It 13 15 17 19 21 23 2S 27 29 311 3 S
■WRIL

1915

MET
mCKittoiriiXAXE,-

NOVEMBER llt.iZmit.V- MNOARY 1918

U 17 19 21 » 2S 27 !9 1 3 S J 9 11 13 IS 17 19 M 23 25 27 2« «■< 3 5 7 9 11

66K31NINI! WITH ,
BIOOB ?U!SMA

24 HRSACe^JiHa

LOWER LIMIT OF
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T-ORCOj

feoiYVT. ON
8**" \ADMXSS1(M1

KE&a
SU&itB

HtAVru

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Date.

Glucose

excreted in

24 hrs.

19J5

gm.

Nov. 16

24.5

" 17

16.7

" 18

31.6

" 19

14.5

" 20

9.3

Dec. 30

3.0

600 Vii-gH"3

rJ

0.3 JO
0.300
0.150
0.20 0

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15 17 19 21 2J 25 27 29
NOVtHaEX

3 5 7 9 11 13 15 17 19 ll 23 2J 27 2« 31-1 3 5 7 9 !1
lECtKBtR MNUAW 1916

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CASE NO.2,496

lBAnKt3510Sl915

JECEMBER
3 5 7 9 II 13 » 17 W a 83-

JUNE savt

» II » is: 17 19 21 23 2! 2.7 » 1 3 S 7

11 a IS 17 19 2! " iS » 49

nrcr
mcALomed

1 WHISKY
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B yROTBIK
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100

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300

400

500

600

700

'«00

900
1,000
1,100
1,200
1,300

1^00

1,SOO |-|--

l,60O

1,700

1,800

i,»oo

2,000

COMWWHS WITH ,

loeec. ■\ ■'5

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Iasmission

6S

3 S 7 9 11 13 IS 17 » 21 »

IICEMBEB

Date.

Glucose

excreted in

241irs.

1st admission.

mis
Dec. 3

gm.
2.0*

18 hr. specimen.

cc.§Aa>
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I output!

blUID

» U 13 13 17 19 21 23 2S 27 29 1

13 15 17 19 31 23 IS » 29

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Chart 51. Case No. 58.

CASH NO. 2,577

i«»AiiwssioN 1915

WET
m CALORIES

0 WHISKT

1 CAKMHTDRXrE

i vRoreiH

D FAT

VE6 JANUAKTlSie

»jH i 5 7 9 n » 15 n 19M a tst? 89

Ml s s 7 9 n 0 15 n » zi !3 w 17 m 3 5 I 9 u u » 3916 tmnna t a 57 9»o

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JULY AOSUST
1916 S)-! 3 5 7 9 U » 15 17 U 21 O 2!
S^AMUSSION

l.:-«wHmii"- ■■" 1

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29»i 3 $ T » ui3un»uiasf aasM 3 5 t » unit »»»»»»»} a

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100
300
400
500
600
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900
1,000
1,100
1,200
1,300
1,400
1,500

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1,700 iz^totalN

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Date.

Glucose

excreted in

24 hrs.

1st admission.

1915
Dec. 29
" 30

8.5*
17.0

2nd admission.

1916
June 21

6.7

■ 8 hr. specimen.

CA51 NO. 2,564

tOACHISUSM 1916

1 3 J 7 9 11 13 IS 17 a J) » IJ J7 » 3H 3 5 7 9 U 13 « J7 19 11 23 SS !7 291 3 S

7 9 IJ n JI n 19 11 !» W 17 » 311 3 5 7

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1916

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9 11 13 15 17 19 21 23 2S 27 29 1 3

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TtBHUAKJ KAXCH AHUl. MAY Saro. WW

JANUARY

rtmiitmi iiw 'mwninwiiiiiiiiwiiin n^

II III 11 III iUmmui mmmm

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9 11 13 15 17 19 21 23 25 27 29 1 3 5 7 3 u 13 IS 17 19 21 23 25 27 29 3W 3 5 7 9 H 13 IS 17 19 21 23 25 !
NOVEMBER DECEMBER JANCWRr 1917

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Chart 53. Case No. 60.

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HOTCMBER DECEMBER. JAUOARV 1317 FtBRUftEY MARCH APRIL

9 11 13 15 17 19 21 23 25 27 29 1 3 5 7 9 H' 13 15 17 19 21 23 25 27 29 31-1 3 5 7 9 II 13 15 17 19 21 23 25 27 29 31-1 3 5 7 9 U 13 15 17 B 21 23 25 27 1 3 5 7 9 11 13 15 17 19 21 23 25 ZI 29 3M 3 5

DIET
IN CALOSrcS

1^1 TOTAL N
8/pElB24HRa

/- LCfWERUMrTOT
J NORMjU. PUISWA
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BODY WT ON
ADMISSION

fHilHil H,l! j i I ^i ]| fllflll iHiHHIIwn lunn iijh myjiHiiiii n iniin iiiini in i i iii imi ii iiii miH.

HORMAL
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U 23 25 27 29 311 3 5 7 9 11 13 IS 17 19 21 43 25 87 29 I 3 5 7 9 11 13 15 1? S 21 23 25 27 29 JM 3 5 7 9 IS 13 15 IT S II 23 25 2? 29 1
AMUL MAY SONS NUt

9 11 13 15 17 19 21 23 25 27 29 1 3 5 7 9 11
KOVEHBER DECEMBER

13 15 17 19 21 23 25 27 29 3H 3 5 7 9 H 13 IS 17 19 21 23 25 27 29 3H 3 5 7 9 II 13 15 17 19 21 23 25 27 1 3 5 7 3 11 13 15 17 19 21 23 25 27 29 311 3 5
JANOARY 1917 TEBRBARY MARCH APRIL

ftCia

'lOiaNE

Date.

Glucose

excreted in

24 hts.

1st admission.

Jan.

" 9

" 10

" 11

" 12

" 13

" 14

" IS

" 16

" 17

" 18

Feb. 9

May 11

28.4*
11.0
9.2
12.1
15.2
14.2
15.3
10.9
12.4
18.3
24.1
18.2
13.8
19.0
20.7
15.1
11 0
2.3
1.6
5.2

12 hr. specimen.

Chart 53. Case No. 60.

Digitized by IVIicrosoft®

CASLNQ 21646

1916 19 21 J3 25 27 29J i

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S 7 9 1115 15 17 19 2125 25 2729 31-1

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100 Ct.

M.OOD flASHA.

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J 5 7 9 11 15 15 IT

19 21 25 25 2? 29 1 5 5 7 9 11 15 13 17 19 21 25 25 27 29 3M

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Date.

Glucose excreted
in 24 hrs.

1916

«m.

Feb.

19

145.0

20

113.0

21

126,0

22

116.0

23

113.0

24

132.0

25

131.0

27

17.0

28

6.0

May

25

14.0

^uRtxe

h !1 53 SS " 2*1 5 5 7 9 « U If 17 IS Jl 55 W J' 2» 'H
ntUMSY MARCH

11 a If 17 19 21 a IS 27 29 J

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9 ]l 13 U 17 19 U » K 37 29 311

JUNE

CASE Na2,6a6

ixMNuuion 1916

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700
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600
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Chart 55. Case No. 63.

dASENaE.620
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TEBHOACT MARCH

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22.3
18.8

8.4

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